The purpose of the study was to characterize the contractility of the transplanted human heart and to evaluate possible adverse effects of denervation or structural changes of the myocardium or coronary vessels. As an index of contractility, the linear slope k of the end-systolic pressure/dimension relationship during afterload increase with angiotensin II was determined by M-mode echocardiography in 34 heart transplant recipients and 20 healthy control subjects. Baseline findings for end-systolic diameter and systolic blood pressure were normal and similar in both groups, but the transplanted hearts performed at a significantly lower end-systolic wall stress (40.4 +/- 12 gm/cm2 vs 49.9 +/- 11 gm/cm2, p less than 0.001). Comparable increase of afterload was achieved in heart transplant recipients with significantly (p less than 0.001) less angiotensin II, which indicates increased vasoconstrictor sensitivity. Contractility index k did not differ between heart transplant recipients (12.95 +/- 4.9 mm/100 mm Hg) and control subjects (12.78 +/- 2.8 mm/100 mm Hg). This finding is consistent with a normal contractility of the transplanted, denervated human heart. Normal baseline contractility therefore is an intrinsic property of the intact heart, which is independent of autonomic neural control. Contractility was not compromised by increasing interval from transplantation or the presence of mild acute rejection or mild interstitial fibrosis. Mildly impaired contractility (k greater than 2 SD of k in control subjects) in four heart transplant recipients (12%) was neither associated with structural myocardial or coronary changes nor with rejection episodes or graft ischemic time. One may speculate that impaired contractility, which is present in a minority of heart transplant recipients, results from pretransplantation damage.