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Systemic alkalosis was used to detect coronary spasm in 237 patients with infrequent, resting, angina-compatible chest pain. The provocative test was performed without previous coronary arteriography but only in patients with negative submaximal exercise test results. Rapid infusion of alkaline solution followed by maximal hyperventilation raised arterial pH above the 7.65 value necessary for diagnostic significance in 196 (83%) patients. In 24 (12%) of these patients the provocative test induced significant ischemic ST segment changes. In all patients with a positive response, coronary artery disease, which was predominantly vasospastic (19 patients) or atheromatous with a vasospastic contribution (five patients), was demonstrated by coronary arteriography followed, if necessary, by ergot derivative injection. Chest pain and ECG changes were always reversed within 5 minutes by intravenous nitroglycerin. Coronary arteriography was not performed in all patients with a negative response; therefore, the sensitivity of the procedure could not be assessed. However, 36 patients with a negative response to hyperventilation underwent coronary arteriography; 33 (92%) had normal arteriograms and a negative response to ergot derivatives. Hyperventilation appears to be a safe and specific diagnostic procedure in a subset of patients in whom the probability of coronary artery disease may not be judged sufficient to warrant coronary arteriography as a primary diagnostic approach.

Twenty patients with pure or prevalent mitral regurgitation, undergone mitral valve conservative surgery according to the Carpenter-technique from 1975 to 1979, have been studied. There are 19 women and 1 man, mean age of 25 years (range 11 to 65); 18 had a rheumatic fever; 2 had a mitral valve prolapse due to a degeneration of collagen within the central core of the cordae tendineae, which was the primarily responsible for cordae rupture in 1 case. The clinical and hemodynamic features were severe in a 50 per cent of cases (8 patients in N.Y.H.A. functional class III; 3 in class IV); there was pure mitral regurgitation in 12, combined mitral stenosis and regurgitation in 8; tricuspidalic regurgitation which needed annuloplasty in 5 patients. All the patients have been studied by hemodynamic and angiocardiographic study before and an average of 14 months after surgical treatment. Surgical conservative technique of mitral valve is described; the results are analyzed. All the patients are in N.Y.H.A. functional class I, 14 months after surgical valve therapy. In three cases, a systolic 3/6 murmur which was present immediately after surgical treatment and that not increased in time, remains. EKG left overload is still present in 2 cases; Heart-Chest ratio decreases in all the patients (range 0,61 to 0,51). Atrial fibrillation is present in 6 patients. Hemodynamic findings show: Pulmonary Systolic Pressure (PSP) decreases (45 +/- 4 to 27 +/- 1); Mean Pulmonary Capillary Wedge (PCW) pressure decreases (19 +/- 1 to 11 +/- 1); Total Peripheral Resistance (TRP) (2023 +/- 112 to 1595 +/- 70 dynes sec cm--5), Total Pulmonary Resistances (TPR) (742 +/- 89 to 351 +/- 36), Pulmonary Arterial Resistances (PArtR) (344 +/- 51 to 133 +/- 18 dynes sec cm--5), and Left Ventricle Diastolic Pressure (LVEDP) (12 +/- 1 to 8 +/- 1 mmHg) normalize. The Ejection Fraction (EF) decreases at the most operative control after surgery in 11 patients (56 +/- 3 to 50 +/- 1). Angiographic study shows no regurgitation in 4 patients, a least regurgitation in 13 cases and there is a 2/4 regurgitation in 3 cases only. The AA. have got to an excellent result in 17 patients; a 2/4 degree angiographic regurgitation persist in 3 cases, although a clear clinical improvement. The AA. consider of great utility this surgical valvular management according to a critical review of the efficacy and stability of the results.

In a fifty-three-year-old man, constrictive metastatic carcinoma of the pericardium revealed a bronchial carcinoma. The subacute course was rapidly progressive. Only partial pericardiectomy could be performed. Death occurred 16 days after the peripheral signs of compression of the heart became patent. In such cases early diagnosis, before signs of constrictive pericarditis become obvious, is very important.

Primary scleroderma myocardial disease may be due in part to myocardial ischemia caused by a disturbance of the coronary microcirculation. We evaluated the effect of the calcium channel blocker nicardipine on myocardial perfusion assessed by thallium-201 scanning in 16 patients with systemic sclerosis. Thallium-201 single photon emission computerized tomography was performed at baseline and 90 min after 40 mg of oral nicardipine. The mean (+/- SD) number of left ventricular segments with perfusion defects significantly decreased from 6.0 +/- 2.0 at baseline to 4.1 +/- 2.3 after nicardipine (p less than 0.01). The mean global perfusion score significantly increased from 10.2 +/- 1.9 at baseline to 11.9 +/- 2.6 after nicardipine (p less than 0.02). Our study demonstrates short-term improvement in thallium-201 myocardial perfusion with nicardipine in patients with systemic sclerosis.

In this review paper, the authors summarize the studies which support the theory that a defect in production of energy by the myocardial cells is a determinant factor in the genesis and/or aggravation of dilated cardiomyopathy. Points that are common to this metabolic theory and to the other pathogenetic mechanisms usually described (notably viral or toxic mechanisms) are presented.