[Hematoma of right ventricular outflow tract mimicking an infiltrating tumor as a consequence of acute aortic dissection]. / Dissecazione aortica acuta complicata da ematoma del tratto di efflusso ventricolare destro.

The aortic dissection may be associated with unusual complications such as fistula formation and vascular compression. We describe a case of a 71-year-old patient admitted to our Hospital because of acute chest pain; transthoracic and transesophageal echocardiography revealed the presence of a type A aortic dissection associated with a mass infiltrating the right ventricular outflow and proximal tract of the pulmonary artery. The ultrasonographic morphology and the surgical findings showed the presence of a hematoma which was consequent to acute aortic dissection and which mimicked a tumor infiltrating the right ventricular outflow.

[Chylothorax following myocardial revascularization with the internal mammary artery]. / Chilotorace dopo rivascolarizzazione miocardica con arteria mammaria interna.

Chylothorax is a rare but serious complication of coronary artery bypass grafting. We describe a case of double myocardial revascularization with the internal mammary artery developing the complication ten weeks after cardiac surgery. The reasons for late symptomatology of lymphatic injury are analyzed. Conservative treatment with low-fat diet, total parenteral nutrition and pleural drainage was attempted unsuccessfully; chyle leakage of around 500 ml/day and onset of nutritional deficiency made it advisable to seal the thoracic duct surgically.

[Posttraumatic pericardial laceration and cleft of the anterior mitral leaflet]. / Lacerazione post-traumatica pericardica e del lembo anteriore della mitrale.

A 17-year-old patient sustained blunt trauma to the chest, during a motor vehicle accident, resulting in a pericardial laceration and cleft of anterior leaflet of mitral valve; both lesions were treated conservatively at a later date. The reasons of late symptomatology of valvular injury and absent initial identification are analyzed. Echocardiography's role for diagnosis, indication and choice of surgical treatment is emphasized.

The combination of chlorthalidone with nifedipine does not exert an additive antihypertensive effect in essential hypertensives: a crossover multicenter study.

To evaluate whether the combination of nifedipine with chlorthalidone exerts an additive antihypertensive effect when compared to single-drug treatment, 66 uncomplicated essential hypertensives, whose diastolic blood pressure was greater than 100 and less than 115 mm Hg at the end of a 1-month washout placebo period, received, according to a randomized, double-blind, crossover design, nifedipine (20 mg b.i.d.), chlorthalidone (25 mg o.d.), the two drugs combined at the same doses, and the corresponding placebo. When compared to the randomized placebo the three active treatments significantly (p less than 0.001) reduced blood pressure without changing heart rate and body weight. However, blood pressure values were similarly reduced under nifedipine and the combination and were significantly lower (p less than 0.05) than those under chlorthalidone. Moreover, the percentage of responders and normalized patients under nifedipine and the two drugs combined were similar and significantly (normalized, p less than 0.0001; responders, p less than 0.02) greater than those under chlorthalidone. Under chlorthalidone and its combination with nifedipine, plasma potassium tended to decrease and blood glucose and serum uric acid were significantly (p less than 0.05) increased. These data show that the combination of nifedipine with chlorthalidone does not exert any additive antihypertensive effect when compared to nifedipine alone and that this combination increases both blood glucose and serum uric acid. Taken together these findings indicate that the combination of a dihydropyridine calcium antagonist with a thiazide diuretic is devoid of any clinical significance in the treatment of uncomplicated essential hypertensives.

Chlorthalidone does not increase the hypotensive effect of nifedipine in essential hypertensives: a crossover multicentre study.

To determine whether the combination of nifedipine + chlorthalidone exerts an additive antihypertensive effect when compared with single-drug treatment, we studied 66 uncomplicated essential hypertensives, with diastolic blood pressure of greater than 100 and less than 115 mmHg. At the end of a 1-month washout placebo period, using a double-blind crossover design, the patients were randomly allocated to nifedipine (20 mg twice a day), chlorthalidone (25 mg once a day), the two drugs combined at the same doses and the corresponding placebo. Compared with the randomly allocated placebo, the three active treatments significantly reduced blood pressure without changing the heart rate or body weight. Both the absolute and percentage decreases in mean blood pressure induced by nifedipine and the combination compared with placebo were similar and significantly greater than those induced by chlorthalidone. Taken together, these data show that the combination of nifedipine + chlorthalidone does not exert any additive antihypertensive effect compared with nifedipine alone. This finding indicates that the combination of a dihydropyridine calcium antagonist + a thiazide diuretic is probably devoid of any particular clinical significance in the treatment of uncomplicated essential hypertensives.

Time-dependent response of coronary flow to prolonged adenosine infusion: doubling of peak reactive hyperaemic flow.

UNLABELLED: In 11 anaesthetised, Open chest dogs the time course and degree of the coronary vasodilating response to intracoronary adenosine infusion was assessed. Continuous adenosine infusion, at a rate of 2.5 to 13.5 mumol . min-1, produced rapid (15 to 30s) vasodilation of the same degree as that evoked by a 30 s period of ischaemia (reactive peak hyperaemia), a finding reported previously by others. However, continuing the infusion led to further coronary vasodilation, reaching a maximum 20 to 45 min from the beginning of the infusion and remaining constant for up to 2 h, independently of further increases in the dose. This late response produced, on average, vasodilatation twice as great as that observed during reactive hyperaemia and was not associated with any haemodynamic change or with the opening of arterio-venous shunts. THE RESULTS: 1) suggest the existence of a double, time-dependent response of coronary receptor(s) to adenosine; 2) demonstrate, in the presence of a prolonged vasodilating stimulus, a possible increase in coronary blood flow to a degree far beyond that of post-ischaemic reactive peak flow, which is generally considered to be the maximal value of coronary blood flow that can be achieved.

Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of "preinfarction" angina.

To investigate the pathogenesis of myocardial infarction we undertook a systematic study of patients with angina at rest, a syndrome known to evolve frequently into infarction. Among 187 consecutive patients, 37 had infarction, all in the area that showed electrocardiographic changes during angina. In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented. In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks. One patient in whom spasm was observed at the onset of infarction died six hours later; at post-mortem examination, a fresh laminar thrombus was found at the site of the spasm. After infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiography.

Coronary vasospasm in angina pectoris.

Coronary angiography was performed during 34 angina attacks in thirty patients admitted because of recurrent angina at rest. Nineteen (seventeen with S-T segment elevation and two S-T depression) had angiograms during a spontaneous attack, eleven (nine with S-T elevation and two with S-T depression) during an attack induced by intravenous ergonovine maleate. Control coronary angiograms showed a wide range of atherosclerotic obstruction, from normal vessels to severe triple-vessel disease. During the anginal attack, all patients with S-T segment elevation had vasospasm localised to one of the major branches, often resulting in complete occlusion. Attacks with S-T segment depression were seen only in patients with double or triple vessel disease, and here the vasospasm generally affected coronary branches without causing complete occlusion. When appropriately searched for, vasospastic angina seems to be common.