Early ventricular fibrillation in patients with acute myocardial infarction: correlation with coronary angiographic findings

To define coronary angiographic characteristics of patientsexperiencing early primary ventricular fibrillation (VF) inthe acute phase of myocardial infarction we studied 266 consecutivepatients without clinical evidence of heart failure. Twenty-sixpatients (group 1) experienced early (< 12 h from the onsetof symptoms of myocardial infarction) primary VF whereas 240patients (group 2) with the same clinical characteristics servedas an appropriately matched cohort. All patients were catheterizedbefore or soon after hospital discharge (1 to 8 weeks afterthe acute event). There was no significant difference in left ventricular ejectionfraction between the two groups of patients (39.6±6%vs 36.9±8%, P = ns). Patients with early VF had a significantlygreater number of diseased vessels than those without VF (3.38±1.05vs 2.03±1.25. P <0.001) and a higher coronary arteriographicGensini score (29.31±4.80 vs 20.16±4.14, P <0.001).The left anterior descending coronary artery was identifiedas the infarct-related vessel in 53.6% of group 1 vs 44.5% ofgroup 2 patients (P <0.05). The mean maximal serum creatinekinase values were not significantly different (1897±1062vs 1426 ±839 IU.l–1, P=ns) between the two groups. These data indicate that patients with early primary VF in thesetting of acute myocardial infarction may have more extensivecoronary artery disease than similar patients without VF. Aworse prognosis could be anticipated for these patients on thebasis of worse coronary anatomy. A more aggressive therapeuticapproach with routine coronary angiography before hospital dischargecould reasonably be justified for patients with early primaryVF complicating acute myocardial infarction.     

Role of Transesophageal Echocardiography in the Diagnosis of Infected Retained Pacing Lead

A 68-year-old woman had a tronsvenous pacemaker implanted 6 years ago. One year after the procedure the pulse generator was removed due to generator site infection. Efforts to remove the lead resulted in fracture of the tip, which was abandoned in the right cardiac cavities. After this the patient suffered intermittent episodes of fever and chills, which responded to antibiotic therapy. At her recent admission, transesophageal echocardiography revealed a large mass attached to the free end of the fractured lead suggestive of the existence of a vegetation on the pacing lead. The diagnosis was confirmed at surgery.     

Acute effect of captopril administration on baroreflex sensitivity in patients with acute myocardial infarction

Depressed baroreflex sensitivity (BRS) after acute myocardialinfarction (AMI) is considered an indication of decreased vagaland/or increased sympathetic tone. To determine the effect ofangiotensin converting enzyme inhibitors (ACEI) on BRS afterAMI we studied 27 patients with a first Q wave AMI, no signsof heart failure and no history of arterial hypertension ordiabetes mellitus. An additional group of10 patients with thesame clinical characteristics served as controls. On the 5thday after the onset of AMI, three consecutive boluses of phenylephrinewere given intravenously and baseline BRS was taken as the meanslope of the linear regression lines of RR intervals over systolicblood pressure. QT interval was also measured and correctedaccording to Bazett's formula (QTc). Consequently, a singleoral dose of captopril 50 mg or placebo was given to treatmentor control group patients, respectively; BRS and QTc were reassessedlh later. One hour after captopril administration BRS increasedfrom 5.95±2.80 to 9.14±3.46ms.mmHg^–1 (P<0.0001);QTc increased from 414±46 to 425± 46 ms (P<0.0001),systolic blood pressure decreased from 125±19 to 115±15mmHg (P=0.0002), while heart rate did not change significantly.Baseline BRS was correlated only with age (r= 0.74, P<0.0001).In the control group, 1 h after placebo, no difference was observedin any variable compared to baseline. Captopril appears to improveBRS immediately in the early phase of AMI.     

The effects of early captopril treatment on left ventricular volumes and function in patients with and without depressed global ejection fraction after acute myocardial infarction

To determine the effects of captopril on left ventricular volumesand function in patients with and without depressed ventricularfunction following acute myocardial infarction (AMI) we studied78 patients with a first Q wave AMI and no clinical evidenceof heart failure. All patients underwent radionuclide ventriculography(RVG) on the 4th day after admission and were then randomlyassigned to receive conventional treatment alone (36 patients,control group) or with the addition of oral captopril, 25 mgthree times daily (42 patients, captopril group). RVG was repeatedone month after the baseline examination. After one month theleft ventricular ejection fraction (LVEF) significantly increasedin the captopril group (from 43.2±1.3 to 50.9±1.6%,P<0.001) and remained relatively unchanged in the controlgroup (from 47±1.3 to 49.2±1.7%, P=ns). In thecaptopril group the subgroup of patients with a baseline LVEF<45% demonstrated a significant decrease in end-systolicvolume index (ESVI) (from 53.3 ±3.2 to 42.4±2.8ml.m^–2,P<0.002) and a highly significant improvement in LVEF (from36.3±1.3 to 49.6±1.8%, P<0.00005). In the controlgroup, LVEF also increased in those in whom it was <45% (from38±1.4 to 42±2.4%, P<0.01), but the increasewas less than that in the captopril group (P<0.01), mainlydue to an increase in end-diastolic volume index (EDVI) (from78.2±4.6 to 84.6±12.3 ml.m^–2, P=ns). Inboth the captopril and control subgroups of patients with abaseline LVEF 45% there was no significant change in LVEF (from50.1±0.8 to 52.1±2.6% and 53.4±1.5 to 54.2±2.1%respectively), but there was a trend for both left ventricularvolumes to increase (EDVI: from 81.4±4.7 to 91.1±9.9ml.m^–2and 76±5.7 to 90.3±9.2 ml.m^–2; ESVI: from40.6±2.6 to 45.2 ±3.4 ml.m^–2 and 32.1±2.6to 40.1 ±3.8 ml.m^–2 respectively, all P=ns). In conclusion, our study confirmed the beneficial effect ofcaptopril on left ventricular size and function in patientswith depressed global LVEF after AMI, but there was no evidenceof a similar effect in patients with preserved global LVEF,at least during the first month of treatment.     

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3.5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4.7 ± 0.5 vs 4.6 ± 0.6 for theleft anterior descending, 4.6 ± 0.4 vs 4.6 ± 0.3for the left circumflex and 4. ± 0.4 vs 4.4 ±0.5 for the right coronary artery (all P=non-significant). Thesubsets of mitral valve prolapse patients with different clinical‘ischaemic’ manifestations were similar in termsof the calculated coronary flow reserve in all three major epicardialcoronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.     

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3·5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4·7 ± 0·5 vs 4·6± 0·6 for the left anterior descending, 4·6± 0·4 vs 4·6 ± 0·3 for theleft circumflex and 4· ± 0·4 vs 4·4± 0·5 for the right coronary artery (all P=non-significant).The subsets of mitral valve prolapse patients with differentclinical ‘ischaemic’ manifestations were similarin terms of the calculated coronary flow reserve in all threemajor epicardial coronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.