# Heart Transplantation > Heart transplantation for NEET-SS Cardiology: recipient selection, donor allocation under NOTTO, immunosuppression, rejection surveillance and CAV. - Canonical URL: https://prepelephant.com/topics/neet-ss/cardiology/heart-transplantation-cardiology - Exam / course: NEET-SS · Subject: Cardiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Heart Transplantation", PrepElephant, https://prepelephant.com/topics/neet-ss/cardiology/heart-transplantation-cardiology ## 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.