ACE-INHIBITORS UNMASK INCOORDINATE DIASTOLIC WALL-MOTION IN RESTRICTIVE LEFT-VENTRICULAR DISEASE

Objective-To assess the effect of ACE inhibition on left ventricular f illing and wall motion in patients with a clinical diagnosis of heart failure. Design-Prospective examination of left ventricular systolic a nd diastolic function using M mode echocardiography and pulsed and con tinuous wave Doppler before and three weeks after starting an ACE inhi bitor. Setting-A tertiary referral centre for cardiac disease equipped with non-invasive facilities. Subjects-30 outpatients with a clinical diagnosis of heart failure in whom treatment with an ACE inhibitor wa s started; age 61 (SD 11) years; 27 male; 3 female; 21 healthy control s of similar age. Results-Left ventricular cavity was dilated both at end systole and end diastole, and fractional shortening reduced. Altho ugh mean isovolumetric relaxation time (IVRT) and transmitral E (early ) to A (late) filling velocity (EIA) ratio were not different from nor mal, a value of 1.0 on the normal frequency plot of the E/A ratio divi ded the patients bimodally into two groups: 20 patients (group A) with E/A ratio > 1.0 and 10 patients (group B) < 1.0. In group A patients, IVRT was short as was transmitral E wave deceleration time compared t o normal (P < 0.001), fulfilling the criteria of restrictive left vent ricular physiology. Left ventricular wall motion during IVRT was coord inate and left ventricular end diastolic pressure was raised on the ap excardiogram (P < 0.001). In group B, E wave deceleration time was lon ger, relaxation incoordinate, and apexcardiogram normal. With an ACE i nhibitor: in group A, left ventricular dimensions fell at end diastole (P < 0.05) and end systole (P < 0.01) but fractional shortening did n ot change; long axis total excursion (P < 0.01) and peak rate of short ening (P < 0.05) both increased; IVRT increased (P < 0.001) with the a ppearance of markedly incoordinate wall motion, minor axis lengthening , and long axis shortening (P < 0.001 for both); A wave amplitude also consistently increased (P < 0.001); finally, transmitral E wave veloc ity fell and A wave velocity increased. ACE inhibition did not alter a ny of the left ventricular minor and long axis or transmitral Doppler variables in patients in group B. Conclusions-Patients with a clinical diagnosis of heart failure differ in their presentation and response to ACE inhibition according to baseline haemodynamics. In restrictive left ventricular physiology, ACE inhibition reduces cavity size and pr olongs IVRT, compatible with a fall in left atrial pressure. At the sa me time, ventricular relaxation becomes very delayed and incoordinate, greatly reducing early diastolic left ventricular filling velocity. T hus ACE inhibition unmasks major diastolic abnormalities in patients w ith restrictive left ventricular disease.