Question 1

In valve repair for heart failure, take a tricuspid valve where the options are a mechanical valve, a bioprosthetic valve or transcatheter edge-to-edge repair (TEER). Which is preferred, and when?

Dr. Biswarup Purkayastha · Accepted Answer

The tricuspid valve is more often repaired than replaced. Even in a moderately aged patient in the 50 to 60 age group, a tricuspid replacement, if necessary at all, would benefit more from a bioprosthetic valve than a mechanical one. The right side of the heart is a low-pressure circuit, so wear and tear on the valve is much less. A mechanical valve in that position carries a very high risk of thrombosis: the gradient across the valve is low, local eddy currents form, and clots develop. If a clot slips into the lung it can cause pulmonary hypertension or pulmonary embolism, in effect a lung stroke, and it can be deadly. The tricuspid valve is therefore best repaired, with a traditional DeVega repair or an annuloplasty ring. If replacement is required, I would place a bioprosthetic valve in anyone older than 40; a mechanical valve in the tricuspid position is highly unlikely.

I would be very wary of TEER, whether the TriClip or its mitral counterpart, the MitraClip. To the surgical community, edge-to-edge repair of the mitral valve (the Alfieri stitch) is the ultimate bailout. There are half a dozen established ways to repair a mitral valve, including sliding annuloplasty and triangular or quadrangular resection. An edge-to-edge repair is reserved for an extreme valve where no repair is possible and replacement is ruled out by financial constraint or an anatomical abnormality. In those cases, I would ask why intervene at all. With today's preoperative planning, including multiplanar three-dimensional reconstruction of the mitral annulus and assessment of annular calcification and mitral annular disjunction (MAD), we can be nearly certain of the anatomy and decide the plan early.

On repair versus replacement more broadly: rheumatic valves do not hold well after repair, and most of the data favouring repair is Western, and even that is changing. A landmark trial in which Marc Gillinov of the Cleveland Clinic was involved, whom I have spoken with personally on this issue, showed that in severe ischaemic mitral regurgitation, replacement gives a more durable correction, with less recurrent regurgitation, than repair; for degenerative valves, a good repair remains durable and is preferred. A health system where patients can return for a re-operation every sixth or seventh year can afford that. Where a rheumatic or ischaemic valve has to have a lifelong fix, replacement is the better strategy scientifically and haemodynamically.

Question 2

What is the place of traditional alcohol in cardiomyopathy?

Dr. Biswarup Purkayastha · Accepted Answer

I would not be the best judge of whether anyone should drink traditional alcohol, but multiple studies have shown beyond doubt that any form of alcohol predisposes to cardiac dysfunction. Traditional drinks have been compared alongside commercially available liquor, and the notion that red wine gives you a healthy heart was debunked long ago. No form of alcohol benefits the heart: chronic consumption will only damage it. Having a drink for a good laugh is a different story, but there is no scientific claim to back the idea that a glass of red wine protects the heart.

Question 3

How do you manage the risk of bleeding when a patient is given a high antiplatelet load of aspirin and clopidogrel?

Dr. Biswarup Purkayastha · Accepted Answer

You do not avoid it. When you load a patient with antiplatelet drugs for an acute coronary syndrome, even without a percutaneous coronary intervention (PCI), you know they carry a higher risk of bleeding, but that is the patient's best protection against further clotting in the coronary artery. What you can do is reduce the risk: give a proton pump inhibitor alongside the two antiplatelets, assess the bleeding risk, use the radial artery for any procedure and keep the combination no longer than needed. You can only control bleeding in a living patient: if the patient dies of a myocardial infarction for lack of treatment, whose bleeding are you going to control?

Question 4

What is the primary indication for using sacubitril/valsartan?

Dr. Biswarup Purkayastha · Accepted Answer

Its primary indication is heart failure with reduced ejection fraction. Sacubitril/valsartan should be started at the lowest possible dose. Because of the Indian patient population I treat, I very frequently start at 25 mg once a day and build up to 50 mg and then 100 mg in weekly steps, as blood pressure, kidney function and potassium allow. In a patient with an ejection fraction below 45%, and especially below 35% with high NT-proBNP levels, I would be very interested in starting sacubitril/valsartan at the lowest dose and building up step by step.

Question 5

From your experience, what is the relative epidemiology of coronary artery disease in Africans, Asians and Caucasians? Are there differences in surgical needs across these populations?

Dr. Biswarup Purkayastha · Accepted Answer

In South Asians, coronary artery disease comes earlier and more aggressively, with a recognised genetic and metabolic predisposition. In Africans, as everywhere else, the main drivers are hypertension, diabetes, smoking, cholesterol, diet and inactivity, which are rising quickly with urban lifestyles. Caucasians are affected mainly because of their diet, sedentary lifestyle and the other ill effects of the developed world. Surgical success rates are very comparable the world over, whether the operation is done in America, Europe, Australia or elsewhere: anything upward of 90%. Across units, pathologies and degrees of severity, I would put the risk of morbidity and mortality after bypass surgery at 5 to 7%, and the same applies to stenting.

Question 6

In patients with HIV and tuberculosis, are there special considerations regarding drug interactions when they undergo interventions?

Dr. Biswarup Purkayastha · Accepted Answer

Tuberculosis itself raises the risk of clots, but anti-tubercular drugs are not a reason to start routine antiplatelet or warfarin; give these only for their usual indications. What matters is the interaction: rifampicin strongly induces liver enzymes and lowers the effect of warfarin and of many cardiac drugs, so warfarin often needs a much higher dose with close INR monitoring. In HIV, many antiretroviral therapies, particularly boosted protease inhibitors and efavirenz, inhibit or induce CYP450 enzymes and interact with a range of cardiac medications: warfarin, some antiplatelets, statins, antiarrhythmics, calcium channel blockers and some beta blockers. Consult the antiretroviral therapy clinic or the infectious disease specialist on the specific interactions of the regimen the patient is on, and alter the cardiac doses accordingly. As a working rule, more often than not the warfarin dose has to go up and the beta blocker dose has to come down.

Question 7

Following up on Dr. Edugbo's question: in an earlier masterclass you suggested the difference in coronary artery disease between Africans, Asians and Caucasians was less about physiology and more about lack of detection and lack of trained manpower. Is that so?

Dr. Biswarup Purkayastha · Accepted Answer

Lack of detection is one factor, but the question was about epidemiology. In South Asians there is a recognised genetic and metabolic predisposition to coronary artery disease; in Africans the main drivers are hypertension, diabetes, smoking and diet. In Caucasians, it is an extremely sedentary lifestyle and fat-heavy food habits: a drink with a huge cheese-loaded burger. There is also a certain amount of heavy meat eating in the African population, and in some Asian populations, which predisposes them. Occurrence is a different matter. The numbers in Asia and Africa are hugely underreported and underrepresented, because quality diagnostic and imaging facilities are not available. If the reported figure is 1 million cardiac deaths a year in sub-Saharan Africa, with the right investigative modalities in place the number would probably be about 3 million. So occurrence is underrepresented, and epidemiologically, South Asian populations are more predisposed to coronary artery disease, while in Africa the burden is rising with hypertension, diabetes and urban lifestyles.

Question 8

Your 2-3-4-5 diet pyramid calls for two legumes, three fruits, four vegetables and five grains. India has a large vegetarian population that is generally perceived to follow this pattern, yet cardiac events have risen over the last two to three decades. How do you explain that?

Dr. Biswarup Purkayastha · Accepted Answer

The age-old Indian diet of two legumes, three fruits, four vegetables and five grains moved from cooking with mustard oil and other naturally sourced oils to cooking with artificial oils, on the promise of added omega fatty acids. Consumers were told that the same oil used to fry fast-food chicken would deliver excellent cardiac health, and because it was packaged well, they believed it. It was omega-3, now it is omega-6, and tomorrow it will be omega-9 or omega-12. Rather than chasing omega numbers, people would benefit far more from going back to traditional olive oil or mustard oil and giving up clarified butter and these modified, omega-loaded, packaged artificial cooking oils. Do that, and you would eliminate half of the heart disease in this country.

Question 9

We often see very fit people, even international athletes such as Shane Warne, suffer sudden cardiac events and death. Does being very fit no longer mean being heart-healthy?

Dr. Biswarup Purkayastha · Accepted Answer

No. Go to any gym and it will ask only for a medical certificate. It will not ask for blood work: not your triglycerides, your homocysteine or your CRP, and it is not concerned with your body fat percentage beyond a handheld gadget. Meanwhile people take large amounts of supplements, most of them non-FDA-approved and unregulated, from a billion-dollar industry selling jars of powders whose contents nobody knows. The focus is on building intense muscle mass, but the heart is also a muscle. A thickened heart muscle in a young athlete has to be checked to tell athletic adaptation apart from hypertrophic cardiomyopathy, an inherited condition and a leading cause of sudden death in young athletes.

Shane Warne, the absolute master of spin, smoked his way through life, ate badly, crash dieted and drank to excess. His was the classic coronary artery disease of the white man, and he had his reasons.

Implantable devices do have a role in preventing death. The Scandinavian footballer Eriksen had a cardiac event on the pitch at Euro 2020 and survived after CPR. He received an ICD and returned to football. For about five years the ICD did nothing; then one day he had an arrhythmia, the device defibrillated him, he felt a little dizzy, walked off the pitch, and was alive. For certain people with cardiac arrhythmias, an ICD can be life-saving.

Athletes also characteristically have a slow heart rate, known as athletic bradycardia, from a combination of hypertrophy, increased vagal tone and other complex physiology, which medicine has recognised for a very long time. With wearable and other monitoring devices, we are now detecting more arrhythmias than ever before: something as simple as an Apple Watch can detect atrial fibrillation, and people have benefited from it.

Question 10

Heart transplant depends on a suitable organ becoming available, and patients wait on an LVAD in between. Can LVADs, or more modern devices, replace heart transplantation altogether?

Dr. Biswarup Purkayastha · Accepted Answer

For people above the age of 55, LVADs have replaced heart transplantation to a reasonable extent, because the LVAD has become destination therapy. For someone who is not a transplant candidate, an LVAD can be a permanent solution, with no immunosuppression, just a simple antiplatelet and anticoagulant. Today's devices can run for 15 years. We currently care for a young man who received an LVAD as a teenager and has lived with it for about a decade. As the device nears the end of its life and develops complications such as battery malfunction, we have registered him with the National Organ Transplant Organization, and he will continue on the LVAD until he receives a heart.

Question 11

Unlike living-donor liver or kidney transplants, a heart has to come from a deceased donor. How far has medical science advanced here, and is there hope from second-generation LVADs?

Dr. Biswarup Purkayastha · Accepted Answer

Three things are going to revolutionise heart transplantation. First, deceased-donor transplantation has to go beyond brain death to donation after circulatory death (DCD). Where a hospital patient who is not brain dead has an unsurvivable illness, the heart itself is healthy, and the family agrees to withdraw life support, the family can be prepared in advance. After life support is withdrawn, the heart stops and a five-minute no-touch period has passed, the heart can be reanimated, retrieved and implanted in a recipient. Many more hospital deaths then become potential donors, and adding DCD to donation after brain death can at least double the donor pool.

Second, machine perfusion: organ transport devices such as the TransMedics OCS keep the heart beating outside the body, with blood pumped in artificially, for at least 12 to 24 hours, well beyond the roughly four hours a cold-stored heart tolerates, while it is transported. Donors much further away then become usable, which also expands the organ pool.

Third, xenotransplantation of hearts from genetically modified pigs into humans has become a reality; I am aware of at least two recipients. Donation after circulatory death, machine perfusion and xenotransplantation are the three developments that will change the deceased-donor transplant space completely in the coming decade.

Question 12

Is there scope for further technological advancement in LVADs?

Dr. Biswarup Purkayastha · Accepted Answer

LVADs have moved from first-generation devices to axial-flow pumps and now to fully magnetically levitated devices with the HeartMate 3, which has minimised stroke, thrombosis and clotting to the point of being a long-term therapy, with about 58% of patients alive at five years. Research is under way on a biventricular total artificial heart. A total artificial heart called the SynCardia exists, and more research is going into a completely magnetically levitated total artificial heart that can be implanted and support both ventricles for years, so that anyone with heart failure could receive the device and get going. But I strongly believe that no device we human beings engineer will be as beautiful as the heart God created, or replace it completely. Heart transplantation is here to stay for at least my remaining active years of practice, another 15 to 25 years.

Question 13

Xenotransplantation has had limited success so far. Is it part of your own practice?

Dr. Biswarup Purkayastha · Accepted Answer

Xenotransplantation is only going to improve with the passage of time.

Question 14

What is the best approach to managing peripheral oedema, swelling of the feet, in a patient with HIV, pulmonary tuberculosis and hypotension?

Dr. Biswarup Purkayastha · Accepted Answer

First obtain a recent echocardiogram and establish the heart function. If the ejection fraction has fallen below 20%, there is no way to manage the peripheral oedema fully: it is there to stay. Diuretics act only up to a limit, and no dose will make the oedema disappear completely. In a failing heart with substantial fluid accumulation, one strategy is a device such as the Aquadex SmartFlow System, a miniaturised ultrafiltration device with a prime volume of about 15 ml that can remove 60 to 100 ml of fluid an hour, at a rate set for each patient. Where the oedema persists whatever dose of diuretic is given, Aquadex may be a logical option. But with an ejection fraction below 20%, this is endgame, and there is little room to offer more. In a hypertensive patient there are more options, such as diuretics or ambulatory peritoneal dialysis, but in a patient with a communicable disease a device in a body cavity that is open to the outside world raises the risk of infection and is not a feasible or acceptable solution.

So in a patient with HIV and bad peripheral oedema, do a quick echocardiogram and be absolutely sure of the ejection fraction. A 20% ejection fraction is a completely different situation from 30%, so have it measured by Simpson's method or another defined method and work from a fixed number. If that number is below 25%, and especially below 20%, there is far less you can offer this heart beyond carefully optimised medical therapy.

Live Discussion with Dr. Biswarup Purkayastha