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The effects of isometric exercise on left ventricular function in 16 patients with chronic coronary heart disease were assessed by measuring left ventricular pressures and volumes under basal conditions and during a sustained effort of 2 minutes 30 seconds at 50% of the maximal effort. In 7 patients (Group I) with abnormal elevation of left ventricular end diastolic pressure (LVEDP) (over 4 mmHg) the end diastolic volume remained unchanged and the diastolic pressure-volume curve was displaced upwards. The ejection fraction fell together with the percentage filling during the first part of diastole with 50% filling occurring after 61% instead of 45% of diastole. The time constant T also increased showing abnormal relaxation. In 9 patients without abnormal elevation of LVEDP on exercise no changes in the other parameters studies were observed. Our results show that pathological elevation of LVEDP during isometric exercise is associated with a decreased ejection fraction and an abnormality of left ventricular relaxation with a reduced rate of filling during protodiastole and an upward displacement of the diastolic pressure-volume curve. The LVEDP alone is therefore an important index of the haemodynamic behaviour of the left ventricle during isometric exercise.

Left ventricular contractile function was evaluated in twenty patients with coronary artery disease before and during handgrip by use of Vpm, VCEIO and Vmax (obtained with a simplified calculation) from high-fidelity pressure measurements. In eight patients the response to handgrip was characterized by an increase of the contractile indices accompanied by small changes of left ventricular end-diastolic pressure (not exceeding + 4 mm Hg) and was considered normal. Twelve patients who showed abnormal or pathologic reaction to isometric exercise repeated handgrip after administration of 0.4 mg of spray nitroglycerin. Thus eight patients normalized their response to exercise, while in four we observed again a pathologic reaction to handgrip. It is concluded that is a useful and simple manoeuvre for a better evaluation of left centricular function in patients with coronary artery disease; the repetition of the test after administration of nitroglycerin can be useful in identifying those patients with greatest contractile reserve.

A 44-yr-old man suffering fro exertional, emotional and spontaneous angina underwent coronary arteriography. During the examination he had a spontaneous attack of angina with ST elevation in the anterior leads. Injection of a contrast medium in the left coronary artery during pain showed marked spasm with anterior descending artery occlusion. The spasm was quickly relieved by nitroglycerin. Intravenous administration of 0.4 mg of ergonovine maleate reproduced the anginal episode with pain, ST elevation in the anterior leads and coronarographic patterns of a spasm occluding the anterior descending artery at the same level. After nitroglycerin, the pain disappeared and the electrocardiographic and coronarographic findings returned to basal conditions.

Screening of patients with precordial symptoms is a mayor social problem. Holter monitoring is easy to use because it ambulatory, non invasive, can be repeated without harm, has no contraindications and permits prolonged monitoring. Therefore, it seemed necessary to determine the "role" of this test. We examined all of the Holter monitorings performed in Dynamic electrocardiographic laboratory of the S. Matteo Polyclinic from 1983 to 1986. 480 of the 3365 patients visited, presented precordial symptoms. 162 patients (group A) had established ischemic heart disease (old myocardial infarction and/or coronary arteriography). 318 patients (group B) had no definite diagnosis. 71 subjects from group A and 140 from group B presented a typical symptomatology. Group A showed a 31.48% positivity during the test with 165 ischemic attacks. Group B had 25.15% positivity with 397 ischemic attacks. 51 symptomatic attacks (30%) were recorded for group B. Therefore, there was a mayor incidence of silent ischemic heart disease in both groups. Results obtained comparing Holter monitoring to the bicycle ergometry exercise test and to functional test, were comparable in 56.91% (sensibility 41.71% and specificity 78.62%) in the first case and 61.38% (sensibility 42.50% and sensitivity 73.77%) in the latter. In conclusion, we believe that Holter monitoring is useful in mass screening because it permits monitoring of most ischemic attacks, whether under stress or at rest, symptomatic or silent.

Four cases of subjects with implanted pacemakers are reported. The patients temporarily presented suspected symptoms of altered activity of the pacemakers. On the other hand usual tests demonstrated a regular activity of the pacemakers. The dynamic electrocardiography, by a regular registration during 24/48 hours and during usual working, documented; once a partial hole in the circuits of the generator, twice a partial break of the catheter, once a displacement. It is underlined the importance of dynamic electrocardiography to identify temporarily altered activity of pacemakers, undiagnosticable by disposable usual tests.

In 6 patients affected by spontaneous angina with S-T elevation and coronariographic findings of obstruction, intravenous administration of ergonovine maleate determined the same clinical and ECG patterns of spontaneous episodes. The coronary arteriography during pain showed a marked spasm with occlusion of a large coronary vessel in four patients. In 2 patients with atypical chest pain and normal coronariogram, E.M. did not induce pain, ECG abnormality or coronariographic alterations. The role of spasm in spontaneous angina is discussed.

31 patients presenting with Prinzmetal variant angina were divided into three groups according to their angiographic appearances. Group I comprised 9 patients with normal or coronary arteries with lesions less than 50% narrowing. Group II comprised 12 patients with single vessel disease. Group III comprised the other 10 patients with significant lesions on two or all three principal arteries. No clinical or electrocardiographical differences were found between the groups as to age, sex or the clinicapresentation of the chest pain. Most patients with normal or nearly normal coronary arteries had normal electrol cardiogrammes between attacjs (8 out of 9) and electrical changes mainly over the inferior wall (8 out of 9). Exercise electrocardiography reproduced ST elevation in 4 of the 9 patients but, in contrast to the patients in the other two groups, never ST depression. However, these features are not specific for patients in Group I as they were observed in 4 patients in the other two groups. Spontaneous or induced coronary spasm were observed in 27 patients, confirming its role as the mechanism of Prinzmetal angina, whatever the anatomical appearance of the coronary tree.

The clinical, electrocardiographic, coronarographic and hemodynamic findings in thirty-one patients with left coronary artery stenosis were compared with those noted in patients with critical stenoses in all the three branches only. It was not possible to distinguish between the two groups of patients by comparing these results, and coronary arteriography is still the only valid diagnostic procedure.

We have seen a case with spasm of the right coronary artery coming on during exercise ergometry in the course of a coronary arteriogram. The patient had angina pectoris spontaneously and on exercise. Bicycle ergometry was repeated four times by the same method, and was positive in three; in two of these there was angina and ST elevation in II, III, aVF, and ST depression in I, aVL and V2 to V5. On one occasion the test was negative, the patient having taken a trinitrin tablet one hour before the test. Repeating the exercise test during coronary arteriography showed spasm of the right coronary artery and elevation of the segment ST in II, III and aVF; this disappeared after trinitrin treatment.

Three patients complained of spontaneous and exertional chest pain, both associated with S-T segment depression in anterior electrocardiographic leads. In each, coronary spasm was demonstrated on coronary arteriography during a spontaneous attack of pain. Coronary arteriograms taken during exercise-induced angina did not show evidence of spastic obstruction; this suggests that exercise-induced chest pain and S-T segment depression were secondary to the increase in oxygen requirements rather than to a sudden decrease in coronary blood flow. Thus, two pathogenetic mechanisms coexisting in the same patient may cause chest pain associated with subendocardial ischemia.

The effects of atrial pacing (A.P.) on the myocardial balance of inorganic phosphate (Pi) were studied in 11 patients with coronary atherosclerosis and pacing-induced angina (Group C) and in 5 normal subjects (Group N). During A.P. in group C 64% of patients had myocardial loss of Pi, statistically significant (p less than 0,025) always with concomitant reduced myocardial extraction or production of lactate, but only 70% of patients with reduced myocardial extraction or production of lactate had myocardial loss of Pi. In only 1 p. of group N myocardial loss of Pi with normal lactate extraction was observed. These data show that during pacing-induced ischemia there is a negative myocardial balance of Pi, that can be used as a metabolic indicator of ischemia, but less reliable than lactate reduced extraction or production.

Based on classifications proposed by Anglosaxon and French authors who were the first to become interested in the so-called cardiomyopathies of unknown origins, 41 cases clinically classified as hypotrophic-hypokinetic (congestive) cardiomyopathies are presented. After a period of clinical observation, 21 cases were studied hemodynamically, with ventriculography and coronaryarteriography, with phonocardiography (35 cases) and follow-up from some months to 6 years. Post mortem studies were performed in 6 patients, five of whom died of congestive heart failure or thromboembolism and one of sudden death. It was concluded that these entities are hypotrophic-hypokinetic cardiomyopathies with a clinical pattern of congestive heart failure and with unknown aethiologic factors. Treatment as far as indications and efficacy are discussed.