Heart Transplantation
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Direct answer
India's first heart transplant was performed at AIIMS New Delhi in August 1994 by Professor P. Venugopal, and in the three decades since, the discipline has grown into a networked programme governed by the Transplantation of Human Organs Act and coordinated nationally by NOTTO. Transplantation remains the gold standard for end-stage heart failure refractory to drugs and devices: indications include inotrope dependence, refractory arrhythmia or angina, peak VO2 below about 12 mL/kg/min, and end-organ dysfunction from hypoperfusion; contraindications include fixed pulmonary vascular resistance above 5 Wood units, active infection or malignancy, and severe irreversible comorbidity. Outcomes are strong — one-year survival of 85-90 per cent and median survival beyond a decade in contemporary registries — but three enemies dominate follow-up: rejection, infection and cardiac allograft vasculopathy.
What you must remember
- Selection numbers: peak VO2 under 12 mL/kg/min (under 14 if on a beta-blocker), LVEF under 25 per cent with declining trajectory, inotrope or mechanical support dependence, and reversibility of pulmonary hypertension — fixed PVR above 5 Wood units is the classic contraindication.
- Indian legal frame: Transplantation of Human Organs Act 1994 (amended 2011), with NOTTO-ROTTO-SOTTO coordinating retrieval and allocation; India's deceased donation rate remains under one per million population — hence long waiting lists.
- Surgery: bicaval orthotopic technique has largely replaced the bi-atrial Lower-Shumway method, with donor ischaemic time ideally under 4-6 hours.
- Immunosuppression: induction (basiliximab or anti-thymocyte globulin) followed by tacrolimus, mycophenolate mofetil and tapering prednisolone.
- Rejection surveillance: serial endomyocardial biopsy graded by ISHLT criteria (3R severe cellular; pAMR for antibody-mediated), with gene-expression profiling as a biopsy-sparing adjunct in selected patients.
- Cardiac allograft vasculopathy: diffuse, distal, rapid coronary disease — the leading cause of late death; screened by angiography, CT coronary or physiology; mitigated by statins, ACE inhibitors and mammalian target of inhibition with everolimus.
- Infection timeline: first month bacterial, months 1-6 opportunistic (CMV, pneumocystis), later community infections and post-transplant lymphoproliferative disorder.
- The denervated heart: no angina, resting tachycardia, blunted chronotropic response to exercise (rate rises late, via catecholamines), and atropine does not work — the physiologically favourite fact.
The first year after transplant
Structure the answer by timeline. Perioperatively, the threats are primary graft dysfunction and right ventricular failure — a recipient's elevated pulmonary pressures meets a donor right ventricle unaccustomed to it — managed with inhaled nitric oxide and inotropes. In the first three months, surveillance biopsies run weekly to monthly; acute cellular rejection is treated with pulsed methylprednisolone, antibody-mediated rejection with plasmapheresis and intravenous immunoglobulin; prophylaxis with co-trimoxazole (pneumocystis) and valganciclovir (CMV mismatch) proceeds alongside. Months three to six bring the opportunistic infection window and steroid-sparing adjustments. Beyond the first year, the agenda shifts to allograft vasculopathy surveillance, malignancy screening (skin, post-transplant lymphoproliferative disorder), renal function under calcineurin-inhibitor toxicity, and adherence — the silent killer of long-term grafts.
The Indian overlay deserves a sentence in any answer: with deceased donation rates under one per million, waitlist mortality is substantial, interstate "green corridor" logistics determine ischaemic time, and lifelong immunosuppression costs run into lakhs of rupees a year, making pre-transplant financial counselling a genuine part of candidate selection.
High-yield viva angles
Three questions recur. "Why does the transplanted patient not feel angina?" — the graft is denervated, so vasculopathy presents as silent ischaemia, arrhythmia or heart failure, never classic pain, and screening is scheduled rather than symptom-driven. "Why does the transplanted heart respond poorly at the start of exercise?" — no sympathetic innervation; cardiac output initially depends on preload (Frank-Starling) and circulating catecholamines, with heart rate rising late. "What does a raised troponin or new dysfunction in year one mean?" — rejection until biopsy proves otherwise. Expect follow-ups on ISHLT grading language (3R, pAMR1R+), the role of gene-expression profiling, and the paradox that India performs only on the order of a hundred heart transplants a year despite its disease burden — an answer that names NOTTO and donation-rate arithmetic reads as well-informed.
Frequently asked questions
What are the standard indications for heart transplantation?
End-stage heart failure refractory to guideline-directed therapy — inotrope or device dependence, peak VO2 below about 12 mL/kg/min, refractory arrhythmia or ischaemia — with no reversible cause.
Which pulmonary haemodynamic finding contraindicates transplantation?
Fixed, vasodilator-unresponsive pulmonary vascular resistance above 5 Wood units, which risks donor right ventricular failure after implantation.
How is rejection monitored?
Serial endomyocardial biopsy graded by ISHLT criteria, supplemented in selected patients by gene-expression profiling and echocardiographic surveillance.
What is cardiac allograft vasculopathy?
Diffuse, accelerated coronary intimal disease of the graft — the leading cause of late mortality — detected by surveillance angiography or CT and managed with statins, ACE inhibitors and everolimus.
How does the denervated heart behave clinically?
Resting tachycardia, absence of angina, delayed chronotropic response to exercise, and insensitivity to atropine — physiology that shapes both rehabilitation and surveillance.