Left ventricular aneurysm presenting with ventricular tachycardia was observed in a 48 year old man. Aetiological investigation was negative. The differences between aneurysm and diverticulum and the aetiologies of aneurysms are discussed. The treatment of the arrhythmias caused by this condition is discussed with the help of a review of the literature.

Dissection of the inferior wall of the right ventricle during the acute phase of myocardial infarction with right ventricular involvement is a mechanical complication which has been recently identified, the diagnosis being almost exclusively post-mortem. The authors report the clinical, echocardiographic and pathological features of myocardial dissection in four patients.Between 1985 and 1988, the diagnosis of myocardial dissection was made by echocardiography in 4 patients aged 77 to 80 years, admitted to hospital for an acute inferior wall myocardial infarction. All 4 patients had signs of acute right ventricular failure indicating right ventricular necrosis and a loud systolic murmur at the left sternal border ; 2 patients were in shock. The ECG showed signs of inferior walt infarction with, in 2 patients, electrical changes suggestive of right ventricular involvement. Echocardiography showed dissection of the inferior wall of the right ventricle as a pulsatile, echo-free space in the diaphragmatic wall of the right ventricle which appeared to obstruct right ventricular ejection in end systole to a variable degree. The outcome was fatal in all cases with death resulting from refractory myocardial failure.Pathological analysis confirmed biventricular inferior wall infarction also involving the posterior part of the interventricular system, the site of a small tear on the left side which communicated with a neo-cavity dissecting the RV posterior wall. The right coronary artery was totally occluded in all cases. The anatomical lesions were fully concordant with the echocardiographic data : the dissection filled with blood from the left ventricle at each systole creating a pulsatile space in the diaphragmatic wall of the ventricle obstructing ejection.

Dissection of the inferior wall of the right ventricle during the acute phase of myocardial infarction with right ventricular involvement is a mechanical complication which has been recently identified, the diagnosis being almost exclusively post-mortem. The authors report the clinical, echocardiographic and pathological features of myocardial dissection in four patients. Between 1985 and 1988, the diagnosis of myocardial dissection was made by echocardiography in 4 patients aged 77 to 80 years, admitted to hospital for an acute inferior wall myocardial infarction. All 4 patients had signs of acute right ventricular failure indicating right ventricular necrosis and a loud systolic murmur at the left sternal border; 2 patients were in shock. The ECG showed signs of inferior wall infarction with, in 2 patients, electrical changes suggestive of right ventricular involvement. Echocardiography showed dissection of the inferior wall of the right ventricle as a pulsatile, echo-free space in the diaphragmatic wall of the right ventricle which appeared to obstruct right ventricular ejection in end systole to a variable degree. The outcome was fatal in all cases with death resulting from refractory myocardial failure. Pathological analysis confirmed biventricular inferior wall infarction also involving the posterior part of the interventricular system, the site of a small tear on the left side which communicated with a neo-cavity dissecting the RV posterior wall. The right coronary artery was totally occluded in all cases. The anatomical lesions were fully concordant with the echocardiographic data: the dissection filled with blood from the left ventricle at each systole creating a pulsatile space in the diaphragmatic wall of the ventricle obstructing ejection.

The results of immediate percutaneous transluminal coronary angioplasty (PTCA) (260 +/- 167 minutes after onset of pain and an average of 56 minutes after thrombolysis) and deferred PTCA (average 9.6 days, range 1 to 30 days after infarction) were compared in 118 consecutive patients with acute myocardial infarction. The overall primary success rate of PTCA was 82.2 per cent; it was higher in those patients undergoing deferred angioplasty (96% vs 78%; p less than 0.05). The primary success rate of immediate PTCA was related to the severity of the stenosis before dilatation: 75 per cent success in occluded compared to 84 per cent in suboccluded vessels (over 90% stenosis) and 100 per cent success in vessels with under 90 per cent stenosis. Eighty one per cent of failed angioplasties occurred in patients with occluded arteries, the majority being left anterior descending (LAD) arteries (71.4%). The incidence of restenosis was 13.4 per cent. This complication was diagnosed at coronary arteriography performed 40 days after PTCA in 1 case, 47 days after PTCA in another case and at the 6 month control in 11 cases. Reocclusion was observed in 21 patients (21.7% of immediate successes). The occlusion was diagnosed at the first control after an average of 8 days in 15 cases. The interval between the onset of pain and thrombolysis and dilatation was significantly longer in the group with reocclusion compared with patients without reocclusion (314 minutes vs 193 minutes for thrombolysis, p less than 0.01; and 356 minutes vs 204 minutes fort PTCA, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Two groups of elderly patients with calcified aortic stenosis were treated by balloon dilatation. In group 1, the valve was dilated just before surgical replacement of the valve. The valvar and annular changes occurring during dilatation were examined visually. In 20 of the 26 patients in this group there was no change. In the six remaining patients mobilisation of friable calcific deposits (1 case), slight tearing of the commissure (4 cases), or tearing of the aortic ring (1 case) were seen. Dilatation did not appear to alter valvar rigidity. In 14 patients (group 2) the haemodynamic gradient across the aortic valve was measured before and immediately after dilatation and one week after the procedure. Dilatation produced an immediate significant decrease of the aortic mean gradient and a significant increase of the aortic valve area. Eight days later the mean gradient had increased and the aortic valve area had decreased. Nevertheless there was a significant difference between the initial gradient and the gradient eight days after dilatation. The initial aortic valve area was also significantly larger than the area eight days after dilatation. The aortic valve gradient rose significantly in the eight days after dilatation and at follow up the gradients were those of severe aortic stenosis.

Numerous studies have been devoted to the effect of slow calcium channel inhibitors on plasma digoxin concentrations. The principal drugs tested, verapamil and nifedipine, were found to increase significantly plasma digoxin levels mainly by reducing digoxin total clearance. Very few studies on the nicardipine-digoxin interaction have been reported. The dual purpose of the present study was to evaluate the influence of orally administered nicardipine on plasma digoxin concentrations over 24 hours and to measure possible variations in the pharmacodynamic effects of digoxin in 9 patients with chronic congestive heart failure. The pharmacodynamic assessment involved simple and cross-sectional echocardiography, systolic time interval measurements and cardiac catheterization. In these patients under chronic digoxin treatment, oral nicardipine had little effect on plasma digoxin concentrations which increased but not significantly; no sign of digitalis toxicity was observed. Nicardipine improved left ventricular function and myocardial contractility by reducing after-load, the nicardipine-induced peripheral vasodilatation tending to counteract the digoxin-induced vasoconstriction.

In a recently published post-mortem series the incidence of cardiac lesions in malignant lymphoma was estimated at about 8.7%. These lesions rarely produce specific cardiac symptoms; they usually are late manifestations of a disease with multiple secondary lesions or are discovered at autopsy. In most patients the lesions are not limited to the heart but represent the extension to that organ of a malignant lymphoma. We observed two cases of cardiac lesions secondary to malignant non-Hodgkin lymphoma and we were able to evaluate their response to chemotherapy. In the first patient the cardiac symptoms revealed the lymphoma; in the second patient the cardiac involvement was discovered 4 years after the lymphoma was diagnosed. In both cases the cardiac lesions were detected by two-dimensional echocardiography. They presented as polypoid masses filling the right atrium and associated with periaortic thickening in the first case, and as a large heterogeneous mass including a tricuspid valve leaflet and extending to the free wall of the right ventricle in the second case. Pericardial effusion was present in the two patients. These echocardiographic findings were confirmed computerized tomography and catheterization. In the first case, followed up for one year, the echocardiographic images reverted to normality after chemotherapy. The second patient, unfortunately, did not respond to chemotherapy and deteriorated rapidly.

Intramyocardial dissecting hematoma is a form of subacute cardiac rupture complicating acute myocardial infarction. Initially contained within the myocardial wall, the hematoma may expand, rupture into adjacent structures, or spontaneously resolve. However, long-term follow-up is unknown because clinical and serial imaging data are lacking. The purpose of this study was to characterize the early and late myocardial wall changes after transmural myocardial infarction using serial ultrasound examinations of the infarct-related segments. Clinical, electrocardiographic, and echocardiographic features of 8 patients (7 men, mean age 59 years) who presented with acute myocardial infarction and echocardiographically documented intramyocardial dissecting hematoma were analyzed. All patients had precordial echocardiography and 6 underwent transesophageal echocardiography. Differentiating hematoma from trabeculations, thrombus, or pseudoaneurysm was done with contrast and color flow Doppler. Seven patients presented with S-T elevation in V1 to V4, and in 3 the elevation extended to V5, V6, I, and aVL. One patient presented with S-T elevation in II, III, aVF, V3R, and V4R. The most striking feature was persistent S-T elevation of more than 72 hours in all patients. Hematoma consisted of a cysticlike, echolucent cavity variable in size, adjacent to severely hypokinetic or dyskinetic infarct-related segments. Hematoma acoustic characteristics depended on time of evolution. Two patients underwent elective revascularization and the rest were medically treated. Two patients died and 6 were alive at the mean follow-up of 12 months. In conclusion, persistent S-T elevation is an important clue in suggesting intramyocardial dissecting hematoma, which is confirmed by its unique ultrasound appearance. Serial echocardiography is useful in determining its evolving nature, and may guide outcome.

Identification of auricular activity is important for the diagnosis of arrhythmias. P waves however are often difficult to recognize. Using M-mode and 2-D echocardiographic techniques, it is often possible to recognize atrial contraction at the level of the atrial septum or of the free wall of the right atrium. Diagnosis can be made in cases of sinus tachycardia, supra ventricular tachycardia with and without aberrancy and ventricular tachycardia with dissociation. Ventricular tachycardia with one to one retrograde conduction or with atrial fibrillation cannot be recognized by this method.

A 67 year old woman was admitted for assessment of asymptomatic aortic stenosis. A large left atrial myxoma was demonstrated by 2D and M mode echocardiography. Coronary angiography was performed as part of the investigation of the aortic stenosis and showed that the tumour depended on the right coronary artery for its blood supply. Careful frame-by-frame study showed the presence of a true right coronary-left coronary fistula through the tumour. The authors discuss the different clinical presentations of left atrial myxomas and their vascularisation in the rare cases in which it has been described.