Archives for December 2018

High Blood Pressure and Headache – Is There A Relationship?

High Blood Pressure and Headache – Is There A Relationship?

Does high blood pressure cause headache? This has been the subject of much debate over the years and the subject of scientific investigation. In this article we will examine the evidence and see if there is an association between high blood pressure and headache. An article about blood pressure guidelines is referenced here.

In General There Does Not Appear To Be An Association Between High Blood Pressure and Headache

Importantly, here we are talking about general increased blood pressure and not a hypertensive emergency (blood pressure higher than 180mmHg) that is discussed a little later. An article outlining some new treatments for extremely high uncontrolled blood pressure is linked here.  Many articles, book chapters and other publications have previously, or continue to report that there is an association between high blood pressure and headaches. It has certainly been documented that very, very high blood pressure can cause headache, but does high blood pressure to a lesser degree cause headache? Many of the early studies that looked at this failed to account for a large number of other possible causes of headache.

Recently better-designed studies have looked at this and most have demonstrated that there is not an association between the high blood pressure and headache. This is even true for moderate or severely elevated high blood pressure. The studies appear to be believable and have used robust methods of blood pressure monitoring including wearable blood pressure monitors.

Can Headache Cause High Blood Pressure?

Patients with active headaches may well have high blood pressures. Of course the physical stress of a headache and any associated pain is an obvious cause of high blood pressure. In these cases, the blood pressure is expected to return to baseline levels once the headache has subsided.

Pheochromocytoma – The Rare Tumor That Causes Extremely High Blood Pressure And Headache

Pheochromocytoma is a rare tumor and a rare cause of uncontrolled very high blood pressure. The classic triad of things associated with a pheochromocytoma is episodic headaches, palpitations and sweating. The headaches are typically associated with palpitations, sweating and anxiety. These symptoms, along with the markedly elevated blood pressure are due to hormones / biochemical substances produced by the tumor. The diagnosis is typically made with blood tests.

High Blood Pressure Crisis And Headache

High blood pressure crisis is known as hypertensive crisis. This is typically defined as blood pressure greater than 180 systolic (top number) and 120 diastolic (bottom number). This is typically a severe uncontrolled episode in patients that usually have a history of blood pressure. Many symptoms can be experienced with the presentation of a hypertensive crisis and typically patients will present to hospital. Headache is one of these symptoms, with others including neurological issues and chest pain. If there is evidence of damage to organs such as the heart, brain or kidney, patients will typically require admission to an intensive care unit and IV medications to control blood pressure.

Pre-eclampsia and Eclampsia – Pregnancy Related High Blood Pressure Headache

Pre-eclampsia and eclampsia are an important, although uncommon cause of uncontrolled blood pressure episodes in pregnancy. High blood pressure, abnormal swelling, and protein in the urine characterize pre-eclampsia. In addition there are a number of other clinical and lab features. Severe and persistent headache is an important part of the disorder. For this reason, the diagnosis should be ruled out in all pregnant women with headache.

High Blood Pressure and Headache – Conclusion

High blood pressure at moderate (140’s) or even severe (160’s) levels are not thought to be a cause of headache; however, dangerously high levels of blood pressure (>180’s) may well be associated with headache as a symptoms. Uncommonly, there may be other conditions that can lead to both high blood pressure and headaches as symptoms.

By

Dr. Ahmed (Interventional cardiologist)

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The New Disappearing Absorb Heart Stent


This is about the Absorb Heart Stent, a new dissolving stent known as a Bio-absorbable Scaffold. Unlike traditional heart stents that remain for life, the Absorb heart stent dissolves over time to where it completely disappears. This has many advantages. In this article myheart.net author, and cardiologist Mustafa Ahmed MD of Princeton Baptist Medical Center, Birmingham, Alabama explains the Absorb stent. Dr Ahmed was amongst the first to implant the commercially available Absorb stent in the US. Dr Ahmed implanted the stent in a patient of cardiologist Dr. Alain Bouchard with a Widowmaker heart blockage at Princeton Baptist Medical Center, Birmingham, Alabama. In this article we present information on the new stent, then we show the story of Mr. Richardson, a patient with the Widowmaker blockage treated with this Absorb dissolvable stent.

What is a Heart Stent?
Heart stents are used to treat blockages in the coronary arteries that supply the heart with blood. A total blockage in a coronary artery would lead to a heart attack, and if not treated rapidly can lead to death of heart muscle. A significant blockage of an artery, usually greater than 70%, can lead to symptoms such as chest pain, shortness of breath and heart muscle damage. Heart stents can be used to treat these heart blockages and open up the artery, relieving the blockage and restoring normal blood supply.

A heart stent is basically a small metal tube that is expanded inside the area of blockage. Once expanded it remains there and acts as a scaffold to keep the artery open. In the old days we used balloons to try and open the artery, but after the balloon was deflated the blockage would often recoil, meaning the chance of a successful procedure was not always good. With the development of heart stents, however, the scaffold from the stent prevented the recoil and meant the artery stayed open.

Problems with Traditional Heart Stents
Although the development of heart stents was a major breakthrough, the presence of these scaffolds within arteries was not entirely without problem. It’s important to remember that vessels are reactive in nature. They expand and constrict in response to various stimuli. This is prevented by metallic heart stents. Vessels themselves are always undergoing changes and the presence of heart stents can disrupt this process known as remodeling. If further work is required in other parts of vessels downstream to the heart stents, the heart stents can get in the way. Metallic heart stents often mean that patients are required to take life long blood thinning medication. These are just some of the problems associated with heart stents, and therefore it was very exciting when absorbable stents were developed.

The absorb stent is known as a bio-absorbable vascular scaffold (BVS) and is a huge breakthrough. The development of the Absorb stent meant that the stent could do its job, but then disappear over time leaving the vessel still open.

For those wishing to dig a little deeper, the science underlying the Absorb heart stent is fascinating. It is made of a bio-absorbable polymer, which is broken down over time. It also releases a drug that prevents early vessel blockages from forming. The stent has three stages before it disappears. These are revascularization, restoration and reabsorption. Revascularization is when the stent is initially placed and restores blood flow in the vessel. In the restoration phase the stent begins to degrade and the vessel regains some of its natural properties. In the reabsorption phase, the Absorb heart stent completely disappears leaving a natural vessel behind.

Studies of the Absorb Heart Stent
The Absorb heart stent has been extensively studied with over 100,000 patients treated as part of trials or registries that have documented its usefulness and safety when used in the right patient population. Followup of up to 5 years has been demonstrated. Importantly, not only does the stent disappear, but also it is comparable in usefulness to existing stents.Some studies showed that if not placed correctly there can be a possibility of stent blockage early on with the Absorb heart stent. It is therefore important to pay attention to detail when placing the stent. The artery needs to be prepared properly and the blockage dilated with the use of good-sized balloons. The artery needs to be of a decent size; the stent is not effective in vessels that are too small. After the stent is placed it should typically be dilated with a balloon that is appropriately sized to the vessel and the stent. Following the suggested protocols can minimize the risk of early stent problems. The Absorb heart stent can be visualized in the vessel using a technique known as optical coherence tomography.

by Dr. Mustafa Ahmed

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Aortic Stenosis a Tight Aortic Valve – A Comprehensive Patient Guide

What is Aortic Stenosis

Aortic stenosis is the medical term used for a tight aortic valve. The aortic valve is the valve through which blood leaves the heart. A tight valve means greater stress on the heart and less blood to the body.  The body needs blood to survive and the heart is responsible for pumping blood around the body. The main pumping chamber of the heart is called the left ventricle. Every time the left ventricle beats it pumps blood out to the body. To leave the heart though, the blood has to go through the aortic valve. The aortic valve is like a door that opens to allow blood to exit the heart and then closes to stop blood from leaking back in. In aortic stenosis the aortic valve is tight and cannot open properly. The tight valve means it’s harder for blood to leave the heart to reach the body where it is needed.

How Does Aortic Stenosis Affect the Heart?

Significant aortic stenosis is a stress on the heart and can lead to symptoms and heart failure and when severe enough can lead to death.  As we said above, the aortic valve is like the door that blood has to go through to get to the body. Imagine that door hardly opened. The body would still need the same amount of blood but the heart would have to work much harder to pump the blood through a tight valve. The heart adapts to this over time and the heart muscle becomes thicker, much in the same way a bodybuilder gets bigger muscles as they life heavier and heavier weights. Unfortunately a thick heart muscle has negative consequences. The heart that used to be able to fill with blood now finds that more difficult because it is so thick. This leads to congestion, and congestive heart failure. The pressures generated by this thick heart are very high, as this is required to allow blood to leave the severely tight valve and reach the body. This may lead to passing out and potentially fatal heart rhythms. Also at some point, the heart will be required to generate such high pressures that it simply gets overwhelmed and fails. At this point the pumping function of the heart can seriously deteriorate and the heart becomes very weak.

What Happens to the Valve In Aortic Stenosis?

In most cases of aortic stenosis the valve becomes thick and full of calcium which can result in severely restricted valve opening.  Decades ago rheumatic fever was the most common cause of aortic stenosis. Rheumatic fever is now rare in the Western world but aortic stenosis is becoming more and more common. This is because people are living longer and longer. Over time the aortic valve is subject to damage and degeneration, wear and tear, almost like joints are more likely to pose a problem in the elderly. This degeneration of the valve results in a process called calcification, which is basically build up of calcium. This calcium build up causes the valve to become less and less mobile, restricting the ability of the valve to open. In severe aortic stenosis, the valve leaflets hardly move and the valve becomes very tight.

When Aortic Stenosis Becomes Dangerous

Severe aortic stenosis is dangerous, particularly when symptoms develop.  Mild aortic stenosis, or aortic sclerosis is not a problem. The heart usually handles moderate aortic stenosis well unless there are other heart problems going on. Problems typically develop when there is severe aortic stenosis however. Although in many people the heart can handle severe aortic stenosis well for a while, at some point the stress will become too much. When patients with severe aortic stenosis develop symptoms or show signs of heart weakness, it’s time to do something. This is because the combination of severe aortic stenosis and symptoms results in a significantly reduced life expectancy. At this point it’s clearly time to fix the valve. Once chest pain, passing out, or heart failure develop, patients with severe aortic stenosis are not likely to survive more than a few years unless the aortic stenosis is treated.

Signs and Symptoms of Aortic Stenosis

Symptoms of aortic stenosis include fatigue, shortness of breath, chest pain, feeling dizzy and passing out.  It’s rare to develop signs and symptoms of aortic stenosis unless the degree of aortic stenosis is severe. Commonly patients may presents with fatigue, the tight valve means it’s difficult to pump the amount of blood the body needs. Fatigue may mean slowing down, reduced levels of activity, or just less energy. Tasks that patients used to do may be much harder. Shortness of breath is another common complaint from patients with severe aortic stenosis. This is a sign if congestive heart failure. There may be swelling also. The high pressures generated by the heart in response to the tight valve may lead to chest pain, particularly on activity. Some patients experience passing out spells; this may be due to dangerous heart rhythms.

Grading Severity of Aortic Stenosis

Grading the severity of aortic stenosis can be challenging and best results are seen from dedicated valve specialists.

Requires Expertise

Although there are criteria for diagnosing aortic stenosis its important to realize that decision making in patients with aortic stenosis is complex. The tests used are not an exact science. Often tests are not accurate and a number of factors need to be taken in to account to come to a conclusion. Many patients with severe disease are misclassified as being less than severe. In the same way some patients have their symptoms attributed to aortic stenosis when in fact the valve is not the issue.

Normal Aortic Valve

As we stated above, aortic stenosis is a tight aortic valve. Every time blood leaves the heart it needs to go through the aortic valve. A normal aortic valve that opens fully provides no obstruction and allows as much blood as needed to leave the heart. Imagine the normal aortic valve area to be as big as the clock face of a medium sized wristwatch. This can be from 3 to 4 cmin area.

Mild Aortic Stenosis

Aortic stenosis is tightening of the aortic valve and mild aortic stenosis is a mild tightening. As we said above the usual aortic valve area is like a medium sized wristwatch around 3-4 cm2 in area. Generally, in mild aortic stenosis, the tight valve remains greater than 1.5-2 cm2. Interestingly, this means the valve isn’t really considered to have mild tightening until it reaches less than half its normal size. Mild aortic stenosis is not of any real significance and does not place strain on the heart or the body. When pressure measurements are taken across the valve in mild aortic stenosis using Doppler ultrasound, a mean gradient of less than 20mmHg across the aortic valve should be measured.  We are able to measure the pressure difference across the valve because as the valve begins to tighten, the blood spurts through the valve at faster and faster speeds, much like when you put your thumb over the end of a garden hose.  Doppler ultrasound can measure this speed and convert it into a pressure drop across the valve, which we can use to define how severe the valve stenosis has become.

Moderate Aortic Stenosis

In moderate aortic stenosis, the valve continues to get tighter. Generally in moderate aortic stenosis the valve area is in the 1 – 1.5 cm2 range. Moderate aortic stenosis is not usually of any significance and does not cause symptoms alone. It is handled well by the body. When pressure measurements are taken across the valve in mild aortic stenosis, a mean gradient of greater than 20mmHg but less than 40mmHg across the aortic valve should be noted.

Severe Aortic Stenosis

In severe aortic stenosis the aortic valve starts to get severely tight. The area of the aortic valve in aortic stenosis is generally less than 1 cm2. This is considered to be a severe obstruction to blood flow leaving the heart and places the heart under strain. Surprisingly patients can handle severe aortic stenosis well and if they have no symptoms this can simply be watched, albeit closely. Once symptoms develop however, the valve needs to be fixed, and relatively quickly. When pressure measurements are taken across the valve in severe aortic stenosis a mean gradient of greater than 40mmHg across the aortic valve should be noted.

Diagnosing Aortic Stenosis

Murmur – Patients with aortic stenosis will have a classic murmur when listened to with a stethoscope over the chest wall. It is a murmur that radiates up to the neck because that is the direction of the blood flowing through the valve as it enters the aorta through the diseased valve.

Pulses – Patients with aortic stenosis have a classic pulse waveform known as parvus et tardus. This means weak and late peaking. It is weak because it’s harder to pump as much blood through the diseased valve, and its late peaking because it takes longer to pump the blood through the tight valve.

Echocardiogram – This is the most important test in confirming the diagnosis and providing the critical information. The echocardiogram is the ultrasound scan test of the heart that gives us pictures of the valve and allows us to take measurements. This will show the tight valve and allow us to calculate a valve area based on pressure gradients through the valve. The echocardiogram also gives us information on the pumping function of the heart and the heart size. This test can also pick up other valve issues such as mitral regurgitation and tricuspid regurgitation. Patients may need a mitral valve repair or mitral valve replacement at the same time if they have a severely leaky mitral valve also.

Transesophageal Echocardiogram – This is an ultrasound scan of the heart, but in more detail, as the probe is passed in to the food pipe (esophagus) where it is close to the heart and can therefore give very clear pictures. This test is very useful in detailing structural heart disease. This allows us to see the valve in great detail and gives us information about other structures within the heart. Often when the normal echocardiogram findings are still unclear, the transesophageal echocardiogram can clarify the issue.

Heart Catheterization – In this test small tubes are passed up to the heart in order to gain information regarding heart pressures and also about the arteries that supply the heart with blood. In general most patients undergoing valve surgery will have a heart catheterization first to make sure no operation is required for the arteries either. Echocardiography is so good now that heart catheterization is rarely used to make a diagnosis of aortic stenosis, however in some complex cases, heart catheterization is used to confirm the diagnosis.

Treadmill Stress Testing – In some patients a treadmill exercise test is used to see the extent of symptoms or functional limitations caused by any aortic stenosis and potentially unmask symptoms patients didn’t know they had.

Stress Echocardiogram – In some cases the diagnosis of aortic stenosis is made difficult by either a weak heart pumping chamber or a small heart cavity. In these cases, standard testing may suggest a moderate tightening when in fact it is functionally severe. For this reason, in these patients, a chemical called dobutamine may be given to speed up the heart rate and the force of contraction, unmasking a severely tight valve of severe aortic stenosis. This is known as a dobutamine stress echocardiogram.

Medical Treatment of Aortic Stenosis

There is no medicine to treat significant aortic stenosis, it is a mechanical problem that requires a new valve to correct it.  As things stand now, aortic stenosis is a problem of the valve itself and there is no medicine proven to prevent aortic stenosis or to reverse the valve tightening. For this reason valve replacement is the preferred treatment option. It’s important to make sure other cardiovascular risk factors are treated in patients with aortic stenosis for a number of reasons. Preventing the progression of other diseases such as artery diseases will improve outcomes. It’s also important to treat high blood pressures in this patient group.

When is it Time to Replace the Valve in Aortic Stenosis?

In general, in significant aortic stenosis, once symptoms develop or there is evidence of heart stress, its time to replace the valve.  The answer is simple: in patients with severe aortic stenosis, once symptoms develop its time to replace the valve. Those symptoms were described a little earlier in this article. In patients with evidence of a weak heart due to the diseased aortic valve, the valve should be replaced even if there are no symptoms. In some cases, when the valve is very severely tight, a case can be made for replacing the valve even in the absence of symptoms.

Another time when the valve would be replaced before symptoms is when patients are undergoing cardiac surgery for some other reason and there is moderate or severe aortic stenosis. Although patients with severe aortic stenosis and no symptoms may be watched without valve replacement, it’s important to watch this group closely because if symptoms develop and they are not treated soon enough outcomes can be poor unless the aortic valve is replaced.

Why Don’t We Just Operate On Everyone With Aortic Stenosis?

In order for a treatment to be justifiable, the risk of the treatment has to be less than simply leaving the disease alone. This needs to take in to account both the short term and the long-term outcomes. In patients with less than severe aortic stenosis its very unlikely the condition will pose a risk. While it is obvious that patients with severe aortic stenosis and symptoms need to have their valve replaced, the situation is less clear in patients with aortic stenosis and no symptoms.

Let me walk you through some of the facts that help influence this decision. The chance of dying due to surgery for aortic valve replacement is around 2.5 %. This includes all patients, from the highest of the high risk to the lowest of the low risk. If we take a 70-year-old patient for example, with no other illness that is coming simply for what we would consider a low risk valve replacement, the chance of dying due to valve surgery is now less than 1%.

This is where it gets interesting. The risk of dying due to the severe aortic stenosis if we were to do nothing is around 0.5 – 1% per year. This approaches the risk of a low risk surgery and so in some circumstances it may be reasonable to consider valve surgery despite the lack of symptoms. On the other hand, in a high risk patient, where the risk of surgery is higher than the risk of simply watching the aortic stenosis, the risk of aortic valve replacement cannot be justified.

In centers of excellence, attention can be paid to risk factors in patients with no symptoms to see who is potentially in a higher risk group. These include patients with abnormal exercise tests, severely thick hearts, very calcified valves, and very tight valves. In patients with one or more of these risk factors it may be reasonable to perform aortic valve replacement in centers of excellence with known good outcomes.

Aortic Valve Replacement Surgery and TAVR procedure

Traditional Open Heart Surgery

Open heart surgery is the traditional method of replacing the aortic valve. The patient is put to sleep under anesthetic and the chest opened down the middle. This is called a sternotomy. Many of you may be familiar with the sternotomy scar that is the scar that runs down the middle of the top half of the chest. In this procedure the heart is placed on a heart lung bypass machine and the heart is stopped. The diseased aortic valve is then replaced with a new aortic valve. The heart is then restarted and the patient taken off the heart lung bypass machine. The in hospital stay will be in the region of a week. By this time most patients will be walking.

Mini Aortic Valve Surgery

This is still open-heart surgery however the incision made on the chest is much smaller than the traditional one. It is just a few inches long. The advantages to a mini approach are a much smaller scar and less trauma with faster healing times. Mini aortic valve replacement is generally the method of choice for the patients of established experts in valve surgery.

Transcatheter Aortic Valve Replacement (TAVR) – The New Revolution

TAVR also known as TAVI or transcatheter aortic valve replacement, is the revolutionary new method of replacing the aortic valve. With TAVR, the procedure is performed without having to place the patient on a heart lung machine. Most TAVR procedures are performed through small tubes that are inserted in to the arteries of the leg. The valve is passed up to the heart through these tubes and placed inside the diseased valve. The valve is then expanded in to place, crushing the old valve out the way and leaving the new valve functioning nicely. The TAVR procedure is outlined in detail in this linked article. In the few patients where TAVR cannot be performed through the arteries of the leg because they are too small or too diseased, then the TAVR is performed through a small incision on the chest wall. Incredibly, in expert centers, some TAVR patients are sent home in as little as 1-2 days after the procedure. Even more incredible is that we are beginning to perform TAVR procedures in patients without even having to put them to sleep.

Ensuring the Best Outcomes – Centers of Excellence

In patients with aortic stenosis, the key is to go to centers of excellence such as Princeton Baptist Medical Center where experts who live and breathe heart valve disease manage the condition. This ensures a number of things. First and foremost is a correct diagnosis and accurate assessment of the severity of the disease. Often this requires the expertise of dedicated imaging experts with expertise in advanced techniques such as cardiac CT scanning and 3D-echocardiography. Expert centers will have the entire range of treatment options available from standard, to mini, to TAVR, to ensure that the appropriate treatment is selected for each patient rather than simply a second best option because that’s all that is available at that place. This way low risk patients are ensured to remain at low risk and the highest risk patients that would have had no option previously are given good options. Expert centers ensure that experienced operators will perform procedures in top class facilities. Centers of excellence ensure no shortcuts are taken and that complication rates remain low. Heart surgery and procedures are a high stakes game. Even in the most routine of cases, unexpected things can happen and situations become critical. It simply makes sense to be in the right place with the right people in that event.

 

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Can heart attack damage be reversed?

 

 

 

 

 

 

One of the most frequent questions our patients ask after surviving a heart attack is: Can heart attack damage be reversed?

Every year, over 700,000 Americans have a heart attack. Improvements in the treatment of myocardial infarction, especially with the reopening of the culprit artery with percutaneous coronary intervention, have led to a large number of heart attack survivors. During the acute phase of the heart attack, the artery is occluded by a thrombus or clot. Below is an example of a patient with a widow maker heart attack. The proximal LAD is completely occluded.

In addition, medical therapy with ace inhibitors/angiotensin receptor blockers and beta blockers can limit certain maladaptive pathways that could lead to infarct expansion. On the other hand, regenerative medicines could lead to shrinking of the scar and prevent the development of clinical heart failure.

Can heart attack damage be reversed? Experimental studies.

In the last decade, the recognition that adult hearts undergo a constant regeneration of its cellular components has created new opportunities for treatment of heart disease. This regeneration machinery resides with stem cells located within the heart. These stem cells can transform into heart muscle (myocytes) or blood vessels (smooth muscle, endothelial cells). In most animal models, the occlusion of an artery leads to damaged myocardium and is replaced by a scar, just like in humans. Zebra fish fully regenerate their heart muscle within 2 weeks after more than 20% of their hearts have been resected. These incredible regenerative properties are also shared by the newt. This enviable regenerative capability has generated a lot of enthusiasm in stem cell research. Various types of stem cells have been used for myocardial regeneration. In this report, we will look atcardiospheres derived cells.

Can heart attack damage be reversed by Cardiospheres derived cells (CDCs)?

Cardiospheres describes a cluster of endogenous cardiac stem cells that form when the cells are cloned. Samples of heart muscle are obtained by biopsies of heart tissue and then grown in culture to yield millions of Cardiospheres derived cells (CDCs) that can later be injected intravenously or intracoronary. These stem cells can differentiate into heart muscle and blood vessels (such as collateral’s seen in patients with coronary disease). Research has demonstrated however, that the therapeutic action of CDCs does not depend on their capacity to engraft and differentiate, but from their ability to stimulate endogenous repair. The release of growth factors triggers regeneration of heart cells and inhibits cell death and fibrosis resulting in improvement in muscle function. In preclinical models of heart attack, they have been shown to reduce the scar size, regenerate cardiac muscle and improve myocardial function.

In a phase 1 clinical trial, CDC autologous (from the same patient) stem cells were obtained from endomyocardial  biopsies of the patients 2-4 weeks after their heart attacks. The CDCs were grown according to the cardiospheres culture method and injected into the infarct related artery one and half to 3 months after their heart attacks. Infarct size was assessed by Magnetic Resonance Imaging (MRI). The patients treated with CDCs showed a reduction in scar mass and increase in viable heart mass and regional wall motion.

Can heart attack damage be reversed by CDCs? the ALLSTAR clinical trial

Obtaining heart muscle tissue with endomyocardial biopsies can be quite cumbersome for the patients. In addition, there are no guaranties of cell integrity. Some cell samples may not be suitable for clinical use. When heart samples are obtained from an Organ Procurement Organization, a master cell bank can be created. Harvested cells grown from this tissue can be used as an allogeneic (other people) version of CDCs or CAP-1002 (Capricor). In preclinical studies, these allogeneic CDCs have been demonstrated to be safe and the efficacy profile of CAP-1002 was indistinguishable from prior studies using autologous CDCS.

The principal goal of phase I/II ALLSTAR clinical trial was to establish the safety of intracoronary infusion of allogeneic stem cells,CAP-1002, in patients with ischemic left ventricular dysfunction (EF less or equal to 45%), 4 to 12 months after a large anterior myocardial infarction.

The secondary objective was to evaluate whether intracoronary infusion of CAP-1002 resulted in structural cardiac or functional clinical benefits in these patients. After a baseline cardiac MRI, patients were randomly allocated to receive CAP-1002 infused through an over-the-wire angioplasty balloon catheter inflated at the start site of the previous blockage of the infarct related artery. Cells were infused over 15 minutes, in 3 boluses of 25 million CDCS each. The angiogram below represents a typical patient enrolled in the study.

The MR imaging protocol is pretty daunting and the adherence to a standardized methodology cannot be overemphasized. For the ALLSTAR study, 30 centers participated and enrolled patients. Enrollment into the study occurred early in our cardiac MR imaging experience . Thanks to the involvement of our radiology department at BBH Princeton with Dr Ricardo Bracer and the radiology technicians, we were able to perform good quality MR imaging studies. Several centers enrolled fewer than 5 patients while some others had more than 15 patients enrolled. In total, 134 patients received the CDC’s and 44 received placebo and underwent follow up MR imaging studies at 6 and 12 months.

For imaging the myocardial infarct, the MRI protocol used a special sequence called Inversion Recovery combined with a contrast agent called Gadolinium (Magnevist in ALLSTAR).  contrast agents do not accumulate in normal intact heart cells (e.g. myocytes) but rather accumulate in the extracellular space or into damaged, rupture myocytes. Therefore, the presence of Gadolinium enhancement can be used to assess infarcts of the myocardium and other myocardial disease.  Ten minutes after bolus injection, delayed images are acquired using a sequential T1-weighted Inversion Recovery turboflash sequence, with a variable T1 delay adjusted for each patient. The optimized choice for Inversion Recovery time “nulls” the signal of the normal myocardium. This optimization also depends on the contrast dose which varies according to the patient’s weight and kidney function. The delayed enhancement images are then obtained 15 mins after intravenous injection with the patient holding their breath for 15 seconds. During that time a minimum of 12 slices covering the whole heart are acquired. Below are the images of our same patient demonstrating a short axis view depicting the infarct (left panel) and where the slice was obtained from the LV (right panel) at baseline and at 12 months in 2 representative levels in that same patient.

Artifacts caused by sub-optimal breath holding technique and patient motion, also referred to as “ghosting artifacts”, can significantly affect the image quality of the study. Inability to obtain an adequate inversion time (T1) can also affect the study, resulting in inadequate nulling of normal myocardium and making detection of abnormal enhancement difficult.  This can result in underestimation of the infarct size or extent of the disease. The presence of metal, such as surgical clips, stents and ICD’s can also cause artifact and degrade the image quality to almost non-interpretable. Some software application can be used to compensate for these artifacts but there are not perfect. Finally, gaps in acquisition through the heart can result in underestimation of the left ventricular mass and/or infarct size. So as you can see, there are a lot of technical and patient factors that can influence the accuracy of infarct size evaluation by MRI.

The ALLSTAR study set out to test whether Cardiospheres-derived cells can reduce infarct size, 3-12 months after a large anterior myocardial infarction. Below represent the infarct at baseline and at 12 months on 2 representative slices on the same patient. The red arrows are pointing to the primary area of the anteroseptal wall  infarction. Notice also a small inner layer of brightness at 2 and 3 o’clock indicating an area of subendocardial infarction involving the anterolateral wall. Finally, the area of increased brightness at 5 o’clock represent a previous infero-lateral infarct.

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Chest Pain in Kids: Explained by a Pediatric Cardiologist

Chest Pain in Kids:  A Common Complaint

Chest pain in kids is a very common complaint that is often heard from young children to teenagers. More often than not it is not a symptom of heart disease in children. In fact, over 95% of children referred to see a pediatric cardiologist for chest pain, do not have any identifiable heart cause.

Parents will appropriately ask what is the cause of chest pain. As there are multiple structures in the chest, there are many different causes of chest pain. I try to think about different causes of chest pain as follows.

Chest Pain in Kids:  Musculoskeletal Causes

Probably the most common forms of chest pain in kids are related to some irritation in the chest wall or the musculoskeletal system. People will use the term growing pains and I think this usually represents costochondritis or inflammation of the joints between the ribs and the breastbone. This usually hurts to push on the chest. As this is an inflammation, using anti-inflammatory medications such as Motrin or Aleve can help. Another common cause is what we term as precordial catch syndrome. I have had this pain and describe it as a sudden and severe pain in the left chest. It will sometimes hurt when I breathe and I’ll try to move to allow the pain to “release”. As quickly as it comes on it will often disappear quickly in a matter of minutes. We are unaware what causes this type of pain, but it is very common and does not seem to be associated with any more severe illness. Sometimes children will also strain or injure the chest wall during sports or workouts. Like other types of soreness, allowing time and over the counter pain medications will allow these symptoms to resolve.

Chest Pain in Kids:  Lung Causes

There are many lung causes of chest pain. Asthma can lead to chest tightness and difficulty catching ones breath. This is a very important cause of chest pain in kids that can be treated and improves ones quality of life. More significant pulmonary causes of chest pain in kids can occur too. Fever and chest pain could represent a lung infection. Severe and persistent chest pain can be a symptom of pneumothorax or air around the lungs. Obviously, severe and persistent chest pain, especially associated with a fever should be evaluated by a physician.

Chest Pain in Kids:  Stomach Causes

Some children will experience chest pain at night while lying down for bed or even wake up at night. As adults, we will feel heart burn after certain meals, children can also experience these symptoms. These symptoms can be treated with antacid medications. And just like stress and anxiety can make people feel uncomfortable symptoms, sometimes children can feel this into their chest.

Chest Pain in Kids:  Cardiac Causes

As I state above, over 95% of chest pain referrals to a pediatric cardiologist are non-cardiac and with that, most are not life threatening. However, there are important cardiac causes of chest pain in children. As with pulmonary causes of chest pain, persistent and severe chest pain, associated with fever can represent pericarditis or an inflammation in the sack the surrounds the heart. Chest pain that occurs repetitively with exercise and symptoms of passing out with exercise can be very important. There are rare coronary artery origin anomalies that can cause these types of symptoms. Other causes can be severe valve abnormalities or hypertrophic cardiomyopathy. In general, many of the cardiac causes of chest pain can be sorted out with good historical evaluations and physical examination and simple tests such as an electrocardiogram and echocardiogram.

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UNCONTROLLED HYPERTENSION INCLUDING HYPERTENSION EMERGENCIES

Uncontrolled hypertension and hypertension emergencies are a powerful risk factor for future cardiac and non-cardiac events. Hypertension affects almost 1/3 of adults and over 1 billion people globally. Hypertension prevalence increases with aging of the population affecting over 50% of people over 60-years old. The new guidelines identified ideal blood pressure, even among the adult and elderly population as lower, and define hypertension as all pressures > 130/80. As a result, almost 50% of American adults will be diagnosed with high blood pressure. The new guidelines established a clinical goal of the adequate treatment of hypertension in all adults, and shared responsibility for delivery of adequate care on both patients and healthcare professionals.

Uncontrolled hypertension and hypertensive emergencies can be categorized:


The calculation of the 10 year risk of heart disease and stroke (ASCVD) using a commonly available the risk calculator which includes the contribution of blood pressure, cholesterol, prior heart or vascular heart disease, diabetes and cigarette smoking.Evidence for organ damage can manifest as chest pain, shortness of breath, numbness, weakness, visual changes or speech problem.

CAD = coronary artery disease, CKD = chronic kidney disease, DM = diabetes mellitus

Uncontrolled hypertension and hypertension emergencies are given emphasis because the higher pressures alone called for a risk to critical organs and failure to treat can result in permanent neurological, cardiovascular and renal damage.

Neurologic end-organ damage can present as hypertensive encephalopathy or intracranial bleed and can manifest as a stroke, loss of consciousness, confusion, seizures, memory loss or visual disturbances. An examination of the eye can show retinal hemorrhage, exudates or papilledema(arrows) as shown below.

Cardiovascular end-organ damage can manifest as back pain in the case of aortic dissection, acute coronary syndrome or myocardial infarction. Acute heart failure usually presents with severe shortness of breath, rales on physical exam and pulmonary edema on the chest x-ray. This can be accompanied by a loss of kidney function in the laboratory testing. Dr. Ahmed found that patients with uncontrolled hypertension have any increased incidence of heart failure if the systolic pressure is greater than 160,  are older or have hypertrophy (LVH) (below is an MRI displaying severe LVH). Patients with chronic kidney disease and systolic blood pressure greater than 140 had an increased risk of mortality and morbidity.

 Treatments :

Uncontrolled hypertensive treatment can be tailored to each patient according to the presence or absence of end organ dysfunction. Some patients with blood pressure > 200/120 can present with symptoms of heart failure and will require immediate IV antihypertensive therapy and observation in the ICU. Sodium nitroprusside can be used and the blood pressure response can be titrated from minute to minute. Esmolol, or labetalol, can also be administered IV and have proven beneficial particularly in patients with aortic dissection and end-stage renal disease.

In contrast, patients presenting with acutely elevated blood pressure (>200/120) without symptoms, and in whom the blood pressure remained significantly elevated at discharge, should be started on medical therapy and follow up closely as an outpatient.

The initial treatment for hypertension should consist of a single drug or combination of 2 drugs (depending on the severity of HTN) from 3 major drug groups. These groups consist of “A, C or D” where A= Ace inhibitors or angiotensin receptor blockers (ARB’s), C= calcium antagonist and D= diuretic, thiazide type. As a rule, blood pressure can be controlled in the majority of hypertensive patients with lifestyle changes and drug therapy with 1 drug in 1/3 of the patients, 2 drugs in 1/3 of the patients and 3 drugs in the final 1/3. Having said that, epidemiological studies have found that control of blood pressures to <140/90 was reported only in 30-50 percent of the patients.

Some patient’s blood pressures remained uncontrolled despite 3 or more medications. These patients have “resistant hypertension” and are at increased risk of cardiovascular and reno-vascular disease. The characteristics of these patients include elderly (>75 yrs), obesity particularly in women and excess dietary sodium. They tend to have concomitant disease including left ventricular hypertrophy, chronic kidney disease, diabetes, and atherosclerotic disease including stiffening of the large blood vessels such as the aorta. Recent studies have shown that predominantly systolichypertension does not respond well to therapy like renal denervation, and suggest that structural factors are predominant.

Uncontrolled hypertension and resistant hypertension treated with the ROX coupler AV anastomosis

The burden of hypertension is considerable, particularly with the large number of patients that cannot be regulated with medical therapies. Lowering blood pressure in average of 10/5 mmHg lowers the risk of stroke by 30-40% and coronary artery disease by 25%. Doubling the reduction of blood pressure can result in a twofold increase in the benefits. New innovative approaches such as the ROX coupler creation of an anastomosis are particularly relevant to patients with uncontrolled, resistant hypertension.

How is the AV anastomosis created using the ROX coupler?

1-     Cross-hair wire localizer

2-     needle and wire advanced from the vein to the artery

3-     Delivery sheath and ROX coupler advance and unfolding of the arterial side

4-     Retracting the venous portion and balloon to size

5-     Final angiogram

How does the AV anastomosis lower the blood pressure?

Routing a small amount of arterial blood into the venous system results in an immediate reduction of blood pressure in all patients by reducing aortic strain and heart’s afterload. This is a mechanical reduction of pressure and is unrelated to the prior use of medications.

The resulting increase in venous pressure increases the filling pressures in the right cardiac chambers and can attenuate the baro-receptor reflex which prevents increases in heart rate as blood pressure falls and limit the sympathetic activation. Also it can result in the hormonal release of peptides that have diuretic and vaso-dilatory affects.  These mechanisms are probably involved in sustaining the lowering of the blood pressure long-term.

How does the AV-anastomosis from the ROX coupler differ from an AV fistula?

The ROX coupler AV-anastomosis is a fixed conduit between the external iliac artery and the vein, and shunts arterial blood into the venous system at a rate of approximately 1 liter per minute. The lowering of the blood pressure is sustained without a rise in heart rate. Local complications such as iliac vein stenosis can present in approximately 30% of patients. Either the loss of the blood pressure benefit or a development of mild thigh edema suggests that this complication has developed. The venous stenosis is treated with local stenting.

The AV fistula created to provide venous access for dialysis patients is an end-to-side anastomosis between the brachial /radial artery with the basilic /cephalic vein. It provides a variable, uncalibrated flow which actually increases over time and can become deleterious, causing an increase in cardiac output, LVH and heart failure.

Preliminary studies with the ROX coupler:

Early testing of the ROX coupler AV-anastomosis device was performed in patients with COPD in an attempt to increase oxygen delivery. While no effects were noted on the level of oxygen in the blood, some patients experienced an improvement in exercise capacity. Hemodynamic studies revealed a decrease in systemic and pulmonary vascular resistance and an  increase in cardiac output and O2 delivery. Moreover, patients with uncontrolled hypertension had a significant drop in both systolic and diastolic blood pressure from a mean of 145/86 to 132/67 at 12 months. The vasodilator effect was greater in patients with more severe baseline blood pressure elevation.

The ROX CONTROL-HTN was a prospective, open-label, multi-center trial in patients with resistant hypertension (>140/90) on a stable regimen of more than 3 hypertensive medications. 83 patients were randomized with 44 assigned to the ROX coupler and 39 continued on medical therapy. After 6 months, a significant reduction in ambulatory systolic blood pressure was seen in the ROX patients with -13.5 +/-18mmHg compared to 0.5+/- 15 mmHg in controls. The 12 month follow up was also encouraging with ambulatory blood pressure reduction being sustained at 15.3 mmHg for the ROX group. Significant diastolic blood pressure reduction was also seen at 12 months pointing to the hemodynamic effects of the AV anastomosis. Particularly interesting was a group similar to our first patient who had failed to respond to renal denervation. Nine patients underwent ROX procedure and had ambulatory blood pressure reduction of 12/14 mmHg at 1 year.

ROX US CONTROL HTN-2 trial:

This is a prospective, randomized, adaptive, double-blind, Sham control, multi-center study to evaluate the ROX coupler in patients with uncontrolled, resistant hypertension. To qualify, systolic blood pressure should be greater than 160 mmHg, or 150 mmHg if a hospitalization was required in the last 12 months. The patients should be on a stable medical regimen that includes a diuretic and 2 additional antihypertensive medications.

 

 

 

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Signs Of A Heart Attack – Explained By A Cardiologist

Signs of a heart attack range from the most classic sign of feeling liken an elephant is sitting on your chest with sweating and arm and jaw pain to less classical signs of a heart attack such as back pain, jaw pain, neck pain, nausea, shortness of breath, palpitations, indigestion, dizziness, and passing out.

The key take away point from this article is that if there is any concern for a heart attack whatsoever, every second counts when it comes to obtaining emergent evaluation. In this article we will discuss signs of a heart attack in more depth from the typical to the atypical in an aim to educate readers about signs of a heart attack and hopefully help save some heart muscle and some lives!

Signs Of A Heart Attack May Differ In Women

It’s critical to recognize that signs of a heart attack may differ in women. In addition to the typical symptom of chest pain a heart attack; women experience other atypical symptoms more frequently than men. This has led to many disparities in care over the years and there is now a strong movement to educate both healthcare providers and patients to be vigilant to this. Whereas men may more frequently experience chest pain as a sign of a heart attack, women may experience back pain, jaw pain, neck pain, nausea, shortness of breath, palpitations, indigestion, dizziness, and passing out.

Signs of a Heart Attack – Chest Pain That May Radiate

Chest pain is the most common and classic sign of a heart attack. It is often poorly localized, but is classically in the area behind the breastbone and associated with a pressure like sensation. The pain may radiate to the neck and jaw and the arms, the left arm most classically with a squeezing like sensation. These symptoms are known as angina. In stable angina these symptoms will often occur with exertion or emotional distress and go away with rest. If the symptoms last more than a few minutes then the diagnosis is certainly not considered stable angina and help should be sought.

Signs of a Heart Attack – Sweating

The medical term for sweating here is diaphoresis, a well-known sign of a heart attack. This occurs due to activation of a defense mechanism known as the sympathetic nervous system, a kind of fight or flight response. The sweating may occur with or without chest pain, and may occur with other non-chest pain symptoms in a heart attack such as arm pain, jaw pain, shortness of breath and such.

Signs of a Heart Attack – Shortness of Breath

In addition to the symptoms mentioned above, or on its own, shortness of breath is well recognized when it comes to signs of a heart attack. This occurs as a manifestation of heart failure caused by heart muscle dysfunction from the heart attack.

Signs of a Heart Attack – Passing out

Passing out may be a sign of a heart attack, and as with other signs or symptoms can occur in isolation or with the other signs mentioned. It may be due to a number of reasons that include a dangerous heart rhythm and low blood pressure. If passing out occurs in a patient with any of the above symptoms, or in a patient with a known history of heart disease, prompt attention is needed.

Signs of a Heart Attack – New Palpitations

Although palpitations on their own are not likely associated with a heart attack, those that newly occur in conjunction with chest pain, sweating and shortness of breath combined are certainly concerning. They may represent simply a fast heartbeat in response to the heart attack, or an arrhythmia directly caused by the heart attack such as ventricular tachycardia.

Signs of a Heart Attack – Shock

The shock referred to here is the process by where the body is unable to compensate for the affects of the heart attack such as heart failure. This generally means the output of the heart is insufficient in terms of what the body needs. Associated symptoms may be light headed and dizziness, a cool and clammy appearance, fast heart rate and low blood pressure. Shock in general would be associated with a pretty large heart attack.

What To Do If Experiencing Signs of a Heart Attack?

The term time is muscle is very relevant here. In the setting of a heart attack, with each minute that passes there is a chance of increasing and often irreversible heart damage. With quick action heart muscle and lives can be saved. If a heart attack is suspected then an ambulance must be called without delay. The patient needs to be taken to a hospital capable of dealing with a heart attack immediately and action taken. On immediate encounter with a healthcare provider, if a heart attack is suspected then medicine such as aspirin will be given without delay. If a STEMI heart attack is suspected then patients will often need to be taken for heart catheterization immediately, ideally within 60-120 minute of initial symptom onset.

Signs Of A Heart Attack – A Summary

Although the classic presentation of a heart attack is chest pain and pressure, radiating to the neck and jaw and left arm with shortness of breath, its important to recognize many patients will have alternative signs and symptoms, especially women. These include back pain, jaw pain, neck pain, nausea, and shortness of breath, palpitations, indigestion, dizziness, and passing out as signs of a heart attack. The most important move if suspecting signs of a heart attack is to call an ambulance without delay as this may well save the life of the person experiencing the heart attack.

 

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Not All Heart Attacks Are Created Equal

Not all heart attacks are created equal. The type of heart attack can influence the prognosis greatly. A heart attack can be recognized by clinical features of chest pain or shortness of breath, ECG or cardiac imaging findings and elevated biochemical markers including the cardiac troponin, the so-called “heart attack blood test”.

The development of ever more sensitive and heart tissue specific cardiac bio markers and more sensitive imaging techniques now allows for detection of very small amount of heart damage or myocardial necrosis. The use of high sensitive troponin assays (used in Europe but not yet in the US) allows for the detection of low levels of troponin even in normal healthy subjects. The majority of cardiac troponin is inside the cardiac cell. The release of cardiac troponin into the bloodstream can involve several mechanisms including cell necrosis, formation of blebs or leakage of the cardiac cell membrane or release of enzymes that can break down troponin. Sometimes rapid heartbeat (tachycardia) or transient myocardial ischemia (angina) can release intact cardiac troponin into the blood.

It is recognized that in the presence of the clinical history suggestive of acute coronary syndrome and ECG abnormality, an elevated troponin result greater than the 99th percentile compared to a reference group is indicative of myocardial necrosis. However, what is more important is those serial troponin measurements can help establish whether the patient’s chest pain is of cardiac origin and whether the patient is having a true myocardial infarction. The patients presenting in the emergency room with chest pain do not all have a myocardial infarction. A higher sensitivity troponin test can help differentiate earlier and more accurately whether the patient is having a myocardial infarction or not. Consequently, serial negative troponin tests have a very good predictive value attesting that these patients can be discharged safely and have a good outcome post discharge. The troponin measurements must be interpreted in the context of the probability of coronary artery disease.

Our 1st patient is a 65-year-old male with diabetes and hyperlipidemia who presented with increasing frequency of chest pain and shortness of breath. His 1st troponin was normal at 0.03 ng/ml. His repeated troponin was only slightly elevated at 0.056ng/ml. He was still having some chest discomfort and he was taken to the cardiac catheterization lab where a severe stenosis of the proximal right coronary artery was recognized and treated with coronary stenting.

Because of the new techniques for detection of MI and the ever evolving treatment of MI, the WHO (World Health Organization) has been updating the universal definition and classification of MIrecognizing the diverse conditions that cause a heart attack. The diagnosis of MI requires evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia. It requires the detection of a RISE and/ or FALL in cardiac troponin with at least one value above the 99th percentile upper reference limit AND at least one of the following: 1) symptoms of myocardial ischemia (chest pain, shortness of breath…), 2) new ECG changes (st segment or LBBB) or development of a Q wave, 3) imaging evidence of MI or new wall motion abnormality (MRI, echo or nuclear), 4) a clot or thrombus by angiogram. Understanding that different types of MI are treated differently, 5 types of MI have been recognized.

TYPE 1 MI

A type 1 MI is a spontaneous MI caused by an atherosclerotic plaque rupture, ulceration, fissuring, erosion or dissection resulting in a formation of clot or thrombus in the coronary artery resulting in the decrease myocardial blood flow and myocardial necrosis. The patient may have underlying severe CAD but on occasion the atherosclerosis can be minimal. These patients can present as STEMI or Non-STEMI. Over the years, treatment with percutanous coronary intervention has been demonstrated to be the best treatment option for these patients. In addition, secondary prevention with anti-platelet therapy and cholesterol treatment has demonstrated significant improvement in the outcome of these patients.

Our next patient is a 61 yo male who developped severe restrosternal chest pain while eating breakfast. The pain persisted all day and he presented to the ER with an ECG showing a right bundle branch block (RBBB) and anterior ST segment elevation (STEMI). Cardiac catheterization revealed a total occlusion of his proximal LAD or widow maker.

The next patient suffered a non-STEMI. She is a 64 yo women with uncontrolled HTN, hyperlipidemia and diabetes mellitus. She presented with intermittent left sided chest tightness radiating to the left arm, accompanied by sweating and extreme weakness. She had several episodes in the last month and, on the morning of admission, she had a 30 minute episode that was more severe than before. In the ER, her ECG showed ST segment depression and her initial troponin measured 0.11 ng/ml. The troponin peaked at 1.99 ng/ml and the angiogram showed critical stenosis of the LAD.

Type 2 MI

A type 2 MI is usually caused by an imbalance between supply and demand. It compromises a diverse group of heart attack patients who have myocardial ischemia secondary to a variety of acute medical or surgical conditions. In these cases, myocardial injury occurs when the myocardial oxygen supply is decreased i.e. severe hypoxemia caused by respiratory failure, severe hypotension, coronary spasm, coronary embolism (below). This patient is a 32 yo men with a past history of hypertrophic non-obstructive cardiomyopathy, ventricular tachycardia s/p dual ICD pacemaker andsevere diastolic heart failure. He presented with mid-sternal chest pain, profuse sweating and severe shortness of breath. A coronary arteriogram 6 months prior showed normal coronaries. His troponin was 3.99 ng/ml and the repeated arteriogram showed total and abrupt occlusion of the marginal branch of the circumflex artery.

Type 2 MIs can happen in patients without coronary artery disease. Currently there is no guidance or consensus on the optimal cardiac investigation, management or treatment strategy for patients. Clinically, one of the main issues is to determine whether the patient had a heart attack at all. Patients admitted to the hospital with all kinds of symptoms get a troponin drawn for different reasons. It should be recognized that patients with advanced age and patients with chronic renal failure, on dialysis, can have chronic myocardial ischemia and chronically elevated troponin. Even if the clinical probability of underlying CAD is high, a final diagnosis of type 2 MI requires the demonstration of a changing troponin value. This is the best way to distinguish between acute or chronic myocardial injury. The 2nd step is to differentiate whether the troponin elevation is reflecting an actual MI versus one that is caused by another reason. A troponin rise with chest pain and new ECG changes usually indicates an AMI. Other causes of troponin rise such as massive or sub-massive pulmonary emboli, pneumonia or myocarditis should prompt the treatment of the primary disease.  A troponin rise in these conditions usually indicates an adverse clinical outcome. Where coronary artery disease is identified, the clinical outcome could be improved with revascularization or medical therapy.

Type 3 MI

A type 3 MI includes cardiac death with symptoms suggestive of myocardial ischemia prior to the death and that presents to the emergency room with new ECG changes including left bundle branch block.

Our patient is a 60-year-old woman with hypertension and smoking history who presented to an outside hospital with back pain and chest pain and ECG abnormality showing ST depression in leads V3 to V6. During the assessment in the emergency room, she developed ventricular fibrillation requiring cardioversion and 3 minutes of CPR. She was transferred to the cath lab where a critical stenosis of the circumflex was treated with percutanous coronary intervention. Her left ventricular function was normal by echocardiography and she did not require an ICD. Her prognosis is excellent.

Type 4.

Type 4 heart attacks are usually related to a percutanous coronary intervention. In patients undergoing percutanous coronary intervention and normal troponin at baseline, an elevation of troponin > 5 x 99th percentile occurring within 48 hours of the procedure, in addition, prolonged ischemic symptoms (>20 mins of chest pain), ischemic ST changes or new Q-wave or angiographic limitation of flow, or new wall motion abnormality usually defines a Type 4 MI.

Another category of percutanous coronary intervention related MI (Type 4b MI) includes stent thrombosis. It is classified as early thrombosis (0-30 days) such as the patient below who had an occlusion of his stent just 6 hours after recanalization of his anterior myocardial infarction. The patient usually complained of recurrent chest pain with ST changes. The mechanisms involved in these circumstances usually entail a malapposition or incomplete deployment of the stent or an edge dissection. The patient was treated with additional stenting and did great.

A late stent thrombosis (31 day to 1 year) can occur when there is a change in the management of the anti-platelet therapy. The case below illustrates an example of an occlusion of the circumflex marginal coronary artery resulting from the patient discontinuing his Plavix just 2 weeks after PCI.  Three months later, he presented with an acute type4 MI.

Type 5 MI.

Myocardial infarctions can occur after CABG particularly when reperfusion is incomplete or the bypass grafts are inadequate to provide myocardial blood flow to the ischemic areas. Other reasons include coronary dissection, global or regional ischemia due to inadequate intra operative myocardial protection. When troponin values are >10 x 99th percentile during the 1st 48 hours following CABG (from a normal baseline), or a new ECG or imaging evidence of MI or documented graft occlusion by cath, a Type 5 MI diagnosis is made.

Our patient is a 48-year-old male smoker, hypertensive, with peripheral vascular disease who had a previous bypass surgery in 2005. The patient presented to the cardiac catheterization laboratory with unstable angina. His angiogram showed a severe occlusion of the left main with diffuse disease of the RCA graft and sub occlusion of the LAD graft. The LIMA was occluded. He underwent redo CABG with right internal mammary artery (RIMA) to the LAD, vein graft to the diagonal branch and a graft to the circumflex OM using the radial artery. The vein graft to the RCA was judged to be adequate and was left alone. During surgery, the patient was found to have severe adhesions, the LAD was small, there was no vein available and the radial artery was noted to have some atherosclerosis. The patient’s course was complicated by respiratory failure, renal failure, blood loss anemia and shock liver. He was placed on full ECMO (Extracoroporeal Membrane Oxygenation), CRRT (Continuous Renal Replacement Therapy), recovered and was successfully discharged. His troponin rose to 18 and resolved to 0.7 at discharge. The patient suffered a type 5 MI and probably would have not survived if he had not been treated aggressively.

In clinical studies, different risks have been associated with different MI subtypes. Type 2 MIs and type 4 or periprocedural MIs have been associated with increased risk of mortality, however, the hazard of death is increased four times after  type 1 or spontaneous myocardial infarction. Although less frequent, patients with 4 MIs or patients with stent thrombosis, whether early or late, and patients with type 5 MIs or post CABG tend to have a worse prognosis with 10-fold increase in mortality. There is a clear adverse effect of all types of MI on mortality. Research is needed to continue to test new medical therapies. We need to emphasize the importance of secondary prevention to reduce the risk of recurrent MI and mortality.

 

 

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