Rupture of the coronary artery after blunt nonpenetrating chest wall trauma detected by color Doppler echocardiography: a case report.

We report a rare case of a ruptured papillary muscle of the anterior leaflet of the tricuspid valve and the rupture of the septal branch of the left anterior descending coronary artery with drainage into the right ventricle after blunt nonpenetrating chest wall trauma. Both abnormalities were detected by transthoracic 2-dimensional and color Doppler echocardiography, and the septal branch rupture was confirmed by coronary angiography. The leading echocardiographic sign of the rupture of the coronary artery was intramyocardial mosaic-colored flow, representing the turbulent high-velocity flow in the ruptured coronary artery. Hypokinesis of the anteroseptal myocardial segments and the presence of Q waves in leads V1 through 4 on the electro-cardiogram were suggestive of anteroseptal myocardial infarction. We conclude that the history of chest trauma, the electrocardiographic changes, and wall motion abnormalities should be stimuli for a careful color Doppler flow "mapping" of the myocardium for possible identification of a coronary artery rupture.

First dose hypotension after angiotensin converting enzyme inhibitor captopril and angiotensin II blocker losartan in patients with acute myocardial infarction.

BACKGROUND: First dose hypotension after the administration of an angiotensin-converting enzyme inhibitor in patients with acute myocardial infarction is one of the most important adverse events of this type of treatment. There is no information about first dose hypotension after angiotensin type 1-receptor blocker in this type of patient. AIM: To compare the first dose responses to low dose captopril and losartan in patients with acute myocardial infarction. METHODS: Single blind, randomised, multicentric, prospective study. Patients (n=320) with confirmed acute myocardial infarction, age >18 years, treated by direct percutaneous transluminal coronary angioplasty, thrombolysis and/or heparin, were randomised to receive a single dose of 6.25-12.5 mg captopril or 12.5-25 mg losartan within 24 h of hospital admission. Baseline laboratory and clinical examinations were performed before entering the study. Blood pressure monitoring started at hospital admission and continued for at least 8 h after the medication (second dose of captopril was given after 8 h). RESULTS: The maximal blood pressure fall appeared about 1 h after the first dose of captopril and 3.5 h after the first dose of losartan. Patients in the captopril group had significantly higher incidence of asymptomatic hypotension (38%) than patients treated with losartan (24%) (P<0.001). No difference in hypotension requiring a change in medication was observed. CONCLUSION: Low dose of losartan is safe for initiating therapy in patients with acute myocardial infarction within 24 h of hospital admission.

A comparison of intervention with losartan or captopril in acute myocardial infarction.

AIM OF STUDY: Angiotensin-converting enzyme (ACE) inhibitors prolong life, lower the progression of heart failure, and decrease the need for hospitalizations in patients after myocardial infarctions. It is still unclear whether these effects could also be achieved by blocking the angiotensin II (ATII) type 1 receptor. METHODS AND RESULTS: We randomized 201 patients with acute myocardial infarction treated with either direct angioplasty, thrombolysis, or heparin alone to the ACE inhibitor captopril or the ATII antagonist losartan. The primary endpoints were safety, tolerability, and left ventricular parameters. The patients were followed for at least 15 days. The incidence of severe adverse events was similar in both groups, although cough presented less often in the losartan group. Captopril failed to prevent an increase in end-diastolic volume and did not influence left ventricular end-systolic volume. This effect led to an increase in the left ventricular ejection fraction (P<0. 001) without a change in wall-motion index. Losartan did not affect end-diastolic volume but decreased end-systolic volume (P<0.001), resulting in a significant increase in left ventricular ejection fraction (P<0.001) and a decrease in wall-motion index (P<0.001). CONCLUSION: This study suggests that losartan is safe and well tolerated in patients after myocardial infarction. ATII antagonists seem to have a more pronounced effect on left ventricular remodeling than ACE inhibitors.

Can dobutamine echocardiography induce myocardial damage in patients with dysfunctional but viable myocardium supplied by a severely stenotic coronary artery?

In animal experiments, dobutamine infusion was found to impair the oxygen supply-demand balance in hypoperfused areas of hibernating myocardium which may induce myocardial damage. The aim of our study was to assess whether dobutamine echocardiography can induce myocardial damage detected by an increase in the cardiac troponin T level in blood. Twenty seven patients with coronary artery disease and severe stenosis of at least one major coronary artery (> or = 90% of luminal diameter narrowing) supplying dysfunctional myocardial segments underwent dobutamine echocardiography. Dobutamine was infused in 3 min dose increments of 5, 10, 20, 30, and 40 microg per kg body weight per minute with the addition of atropine up to 1 mg if ischemia or an 85% predicted maximal heart rate were not achieved. In 15 patients the protocol with prolonged application of 40 microg per kg per minute of dobutamine for 6 min and for the next 5 min with the addition of atropine was used. To exclude minor myocardial damage, an increase in the cardiac troponin T blood level was assessed qualitatively by the TROP T sensitive Rapid Test 20 h after dobutamine echocardiography. In 20 patients the dysfunctional segments were found to be viable with inducible ischemia exhibiting either continuous worsening in systolic thickening or "biphasic" response characterised by the improvement of their systolic thickening with a small dose and by a worsening of the thickening with a high dose of dobutamine. No patient exhibited positive TROP T sensitive Rapid Test result. In patients with coronary artery disease and severe stenosis of a major coronary artery supplying dysfunctional but viable myocardial segments, dobutamine echocardiography does not induce myocardial damage detectable by an increase in cardiac troponin T level.