Preinfarction angina prevents left ventricular remodeling in patients treated with thrombolysis for myocardial infarction.

BACKGROUND: It has been shown that preinfarction angina may have beneficial effects on infarct size and mortality. However, there are no studies that have serially assessed the impact of preinfarction angina on left ventricular (LV) function in a large series of patients. HYPOTHESIS: The study was undertaken to determine whether preinfarction angina (within 7 days before infarction) influences LV remodeling. METHODS: In all, 119 consecutive patients with acute myocardial infarction were serially evaluated by 2-dimensional echocardiography (on Days 1, 2, 3, and 7; at 3 and 6 weeks; and at 3, 6, and 12 months following infarction). Left ventricular volumes were determined using Simpson's biplane formula and normalized for body surface area. Wall motion score index and sphericity index were calculated for each study. Coronary angiography was performed before discharge. RESULTS: Preinfarction angina was detected in 39 of 119 patients. Initial echocardiographic and clinical data as well as the incidence of patent infarct-related artery and collaterals were similar for patients with and without preinfarction angina. In the subset of thrombolysed patients, patients with preinfarction angina showed decrease of LV end-diastolic and end-systolic volumes during the follow-up period (p = 0.033 and p = 0.001, respectively), and improvement of wall motion score index (p < 0.001) and ejection fraction occurred (p = 0.001), without changing of LV shape (p > 0.05); in addition, patients with preinfarction angina had smaller LV volumes and higher ejection fraction than did those without angina, from 3 weeks onward. These favorable effects were not detected in patients not treated with thrombolysis. CONCLUSIONS: These data indicate that preinfarction angina has an inhibiting effect on long-term LV remodeling in patients who underwent thrombolysis for first acute myocardial infarction. It appears that preinfarction angina has no impact on infarct size and early postinfarction LV function.

Isolated mitral regurgitation complicating relapsing polychondritis.

The reported incidence of mitral regurgitation in relapsing polychondritis ranges from 2 to 3% and is associated with aortic regurgitation. There are no reports that mitral regurgitation can be an isolated cardiac complication of relapsing polychondritis. This case report demonstrates that partial chordal rupture and consequent severe mitral regurgitation can be the only features of cardiac involvement in relapsing polychondritis.

Association of ventricular arrhythmias with left ventricular remodelling after myocardial infarction.

OBJECTIVE: To assess the relation between ventricular arrhythmias after myocardial infarction and left ventricular remodelling. DESIGN: Prospective study with consecutive patients. METHODS: 97 patients with acute myocardial infarction underwent serial echocardiographic examinations (days 1, 2, 3, and 7, and after 3 weeks) to determine end diastolic volume, end systolic volume, and ejection fraction; volumes were normalised for body surface area and expressed as indices. Holter monitoring was performed on the day of the final echocardiogram. Coronary angiography was performed in 88 patients before hospital discharge. RESULTS: Complex ventricular arrhythmias (defined as Lown class 3-5) were found in 16 of 97 patients. In logistic regression models, variables predictive of complex ventricular arrhythmias were end systolic volume index on admission (b = 0.054, P = 0.015) and end diastolic volume index after three weeks (b = 0.034, P = 0.012). Complex arrhythmias were also related to the increase of end diastolic and end systolic volume indices throughout the study (F = 5.62, P = 0.046, and F = 6.42, P = 0.017, respectively by MANOVA). A two stage linear regression model of ventricular volume versus time from infarct showed that both intercept (initial volume) and slope (rate of increase) were higher for patients with complex arrhythmias in both diastole and systole (P < 0.001 for all). CONCLUSIONS: Complex ventricular arrhythmias after myocardial infarction are related to the increase of left ventricular volume rather than to depressed ejection fraction. Complex arrhythmias may be an aetiological factor linking left ventricular remodelling with higher mortality, but larger follow up studies of patients with progressive left ventricular dilatation after myocardial infarction are necessary to answer these questions.

Detection of massive pulmonary embolism by transesophageal echocardiography.

Transesophageal echocardiography is a new echocardiographic technique with indications that are still expanding and being redefined. Recently, the usefulness of transesophageal echocardiography in pulmonary embolism has been demonstrated in several case reports. In this article, we present 3 cases with pulmonary embolism diagnosed by transesophageal echocardiography and discuss its diagnostic value in this clinical setting.