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One hundred eight consecutive patients with proved coronary artery disease and reproducible exercise-induced myocardial ischemia were studied. During repeated exercise testing, 52 patients (Group I) had myocardial ischemia in the absence of pain (silent ischemia) whereas 56 patients (Group II) experienced anginal symptoms in the presence of electrocardiographic signs of ischemia. A pulpal test was carried out in all patients using an electrical dental stimulator commonly used in dentistry. Electrical current was delivered in increasing intensity from 10 to 500 mA, and the dental pain threshold and the reaction of the patients to maximal stimulation were determined. During the pulpal test, 71.2% of the patients in Group I did not experience pain, even at maximal stimulation (threshold 0), 11.5% were sensitive at threshold I (10 to 200 mA) and 17.3% felt pain at threshold II (210 to 500 mA). In Group II, 69.7% of the patients complained of dental pain at the low intensity test current (threshold I), 10.7% at threshold II and 19.6% at threshold 0. In Group I, 71.2% of patients did not have discomfort (reaction -), even at maximal stimulation, 21.1% had a mild reaction (reaction +) and 7.7% had an intense painful reaction (reaction ++). In Group II, 80.4% of patients were sensitive to the pulpar test (67.9% reported intense painful sensation at maximal stimulation, 12.5% had a mild reaction); 19.6% of patients had no reaction. The two groups of patients were similar with respect to age, sex and angiographic features.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Unlabelled: To investigate the incidence of myocarditis, 30 patients, with unexplained congestive heart failure, underwent endomyocardial biopsy. For each case three to five samples were examined on light and electron microscopy. Inflammatory infiltrates and injury to adjacent myocytes consistent with myocarditis were detected in 3 of the 30 cases (10%). Changes attributable to cardiomyopathy were found in the remaining 27 cases. Two of the three patients with biopsy-proven myocarditis were treated with prednisone and azathioprine. Their control biopsies six months later showed interstitial fibrosis and absence of inflammatory infiltrates. They clinically improved but hemodynamic and angiocardiographic patterns failed to show the expected improvement. The third patient affected by myocarditis died two weeks later., In Conclusion: in our series of patients with unexplained congestive heart failure, the incidence of biopsy-proven myocarditis resulted low (10%). The results of the immunosuppressive treatment in two patients with myocarditis were unconclusive. Therefore the effectiveness of such therapy should be confirmed in a larger number of patients.

We thought chest pain associated with ST segment elevation during exercise test in patients with not significant coronary lesions could be related to coronary spasm. Three patients with mild coronary obstructive lesions underwent coronary arteriography during exercise test. In two patients this hypotesis was supported by angiographic documentation of the coronary spasm.

The purpose of this study was to focus on the clinical and angiographic characteristics of 113 patients with crescendo angina (Group I) as compared to 187 patients with angina of new onset (Group II), selected from a series of 474 consecutive subjects, admitted to our clinic between January 1976 and July 1983 because of recurrent episodes of spontaneous angina, who underwent cardiac catheterization and coronary angiography within one month of hospitalization. Group I patients showed a greater incidence of prior transmural myocardial infarction (p less than 0.01), arterial hypertension (p less than 0.01), multivessel disease (p less than 0.01) and a lower value of left ventricular ejection fraction (p less than 0.01) than Group II patients. In the latter group of patients anginal episodes were more frequently associated with S-T segment elevation than with S-T segment depression (p less than 0.001), while the opposite was found in patients with crescendo angina. Survival curves up to five years showed that medically treated patients with crescendo angina had a worse long-term prognosis than patients with unstable angina of new onset (p less than 0.01). On the contrary no difference was found between the surgically treated patients of the two groups. Our data suggest that the more diffuse involvement of the coronary tree associated with a more depressed left ventricular function may result in an unfavorable long-term prognosis in patients with crescendo angina as compared to those with unstable angina of new onset. Such a difference between the two groups was abolished by surgical treatment.

Exercise-induced silent myocardial ischemia is a frequent feature in patients with coronary artery disease. The purpose of this study was to compare the clinical and angiographic characteristics of 269 patients who complained of chest pain during an exercise test (group I) with those of 204 who developed exercise-induced silent myocardial ischemia (group II). Group I patients more frequently had anginal symptoms of class III and IV of the Canadian Cardiovascular Society than did group II patients, who had milder symptoms (p less than 0.001). The only angiographic difference observed between the two groups was a slightly but significantly higher left ventricular end-diastolic pressure in group II patients (p less than 0.05), who also showed a longer exercise duration (p less than 0.01) with a higher heart rate-systolic pressure product (p less than 0.01) and more pronounced ST segment depression at peak exercise (p less than 0.001). Moreover, ventricular ectopic beats during exercise were more frequently observed in group II patients (p less than 0.05). Coronary bypass surgery was performed in 45% of patients of group I and in 24% of patients of group II (p less than 0.05). Survival curves of medically treated patients did not show any statistically significant difference between the two groups. Thus, although patients with a defective anginal warning system may have more pronounced signs of myocardial ischemia and a greater incidence of ventricular arrhythmias during exercise, their long-term prognosis is not different from that of patients who are stopped by angina from the activity that is inducing myocardial ischemia.

Five patients affected by angina pectoris showed a spontaneous attack of myocardial ischemia in the course of coronary arteriography examination. During the ischemic episode it was shown a severe coronary arterial spasm promptly relieved by nitroglycerin. In these patients the administration of ergonovine maleate induced the same clinical, electrocardiographic and coronariographic patterns of spontaneous ischemic episodes. These data support the hypotesis that the ergonovine maleate administration is a suitable test for detection of the vasospastic pathogenesis in acute myocardial ischemia.

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.

Thirty patients with myocardial infarction were studied using Digital Subtraction Ventriculography with Intravenous injection (DSVIV) between 3 and 6 days from myocardial infarction and were checked after 30 and 90 days. The variation of ejection fraction in the controls was not important. The wall motion provided precise indications regarding the infarctual regions. Digital subtraction ventriculography seems to be a very interesting tool in the study of the left ventricle in the evolution of myocardial infarction, thanks to a low invasivity, providing data on ventricular function.

This report addresses the problems related to surgical treatment of post-infarction ventricular tachycardia (VT) and is based on a 5 year experience of 36 consecutive patients. In every case the arrhythmia was unresponsive to pharmacological therapy. All patients were operated on after the completion of a diagnostic protocol including preoperative endocardial, intra-operative epi-endocardial mapping, the latter performed automatically when possible. Surgical techniques were: classical Guiraudon's encircling endocardial ventriculotomy (EEV); partial EEV, endocardial resection (ER); cryoablation or a combination of these procedures. The in-hospital mortality (30 days) was 8.3% (3 patients). During the follow-up period (1-68 months), 3 patients (9%) died of cardiac but not VT related causes. Of the survivors, 92% are VT-free. We consider electrophysiologically guided surgery a safe and reliable method for the treatment of post-infarction VT and suggest its more extensive use. We stress the importance of automatic mapping in pleomorphic and non-sustained VT, and the necessity of tailoring the surgical technique to the characteristics of each case.

The aim of this study was to compare the pharmacokinetics and antiarrhythmic activity of dihydroquinidine and quinidine in 14 patients (11 men, 3 women, aged 28 to 67 years) with heart disease and chronic, stable, high-frequency premature ventricular beats (PVB) (greater than 100/hr). A randomized, double-blind, crossover, placebo-controlled protocol was utilized. During Holter monitoring the patients were given either dihydroquinidine or quinidine as the gluconates in an oral solution (600 mg); blood samples were taken 0.5, 1, 1.5, 2, 4, 6, 8, and 12 hours later. The patients were then assigned to three successive treatment periods of 7 days each: dihydroquinidine HCl (900 mg/day), quinidine polygalacturonate (1,650 mg/day), or placebo. At the end of each period 24-hour Holter monitoring was carried out and a blood sample was taken for determination of drug concentration. By comparing the area under the curves dihydroquinidine was 59% as available as quinidine; rates of absorption and elimination were similar. Mean peak blood levels of dihydroquinidine and quinidine were 1.06 +/- 0.34 and 2.15 +/- 0.96 micrograms/ml, respectively. After dihydroquinidine, eight patients had a positive response (greater than 50% reduction in PVB frequency), while seven patients responded to quinidine. During maintenance treatment both dihydroquinidine (233 +/- 330) and quinidine (234 +/- 311) reduced the mean PVB frequency per hour compared to placebo (690 +/- 569). Nine patients (64%) on dihydroquinidine and eight (57%) on quinidine had greater than 70% decrease in mean PVB frequency per hour. Steady-state peak plasma concentrations of dihydroquinidine and quinidine were 1.10 +/- 0.41 and 2.24 +/- 1.13 micrograms/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

The Authors discuss their research on 800 endocardial permanent pacemakers (ventricular, atrial, and bifocal) implanted during six years. In the light of the examination of the literature, the AA. report the complications registered, in particular: lead's displacing 6.2%, run away 0.7%, marked hyperthermya 0.0%, haemorrage 0.4%, wound dehiscence 0.3%, asectic necrosis by decubitus 5%, septic necrosis 0.3%, perforation of the heart 0.2%, pulmonary embolism 0.1%. Both the most common causes of complications and the technical expedients employed to minimize the complication rates are being discussed.

Left ventricular pseudoaneurysm is a rare condition which may develop after rupture of the ventricular myocardial wall. A localized hemopericardium confined is then formed outlined by the parietal pericardium. The pseudoaneurysmal sac is formed by clots and fibrous pericardial tissue and is directly connected to the ventricular chamber. There are no specific clinical signs to identify the disease. Two dimensional echocardiography and computerized tomography can allow the correct diagnosis to be made before cardiac catheterization. Two cases of left ventricular pseudoaneurysm occurring one after chest trauma and the other after acute myocardial infarction are reported.

In order to determine those factors which influence long-term prognosis in patients with angina at rest associated with transient ST-segment changes, 217 patients undergoing medical treatment were followed for a mean of 39 months. All patients underwent coronary arteriography. Univariate analysis identified 12 variables significantly related to prognosis. These were disease of the left main coronary artery; the number of diseased vessels; left ventricular end-diastolic pressure; ejection fraction; baseline electrocardiogram; presence of prior myocardial infarction; ST-segment depression and ventricular arrhythmias during pain; disease of the proximal anterior descending coronary artery; crescendo angina; hypertension; and age. Use of the Cox regression model for survival analysis revealed only 3 variables which were independent predictors of prognosis. They were disease of the left main coronary artery; the number of diseased vessels and left ventricular end-diastolic pressure. The model allowed stratification of patients into 3 groups. Survival at 3 years was 98% in the low risk group; 82% in the intermediate risk group; and 58% in the high risk group. These data indicate that disease of the left main coronary artery, the number of diseased vessels and left ventricular end-diastolic pressure are the independent predictors of prognosis in angina at rest. These variables may allow stratification of patients into groups having different long-term survivals.

In 9 of 12 patients who underwent cardiac transplantation computed tomography was performed. In 5 of them CT was obtained also before the surgical treatment. In all patients angio-CT technique was performed, while the ECG-gated technique was employed only before surgery. CT shows changes in morphology of both atria but over all of the right one, and rotation of the heart on the longitudinal axis. The conditions of the pericardium are particularly well demonstrated: in 5 cases pericardial effusion was observed, 3 times localized and 2 times diffuse. Only in 1 patient a small thrombus in the right atrium was demonstrated. CT allows the possibility to obtain simultaneously information on mediastinum, lungs and pleura. Pleural effusion, pulmonary infections and mediastinal complications are easily demonstrated.

Ergonovine testing was carried out in a selected group of 25 patients with Prinzmetal's variant angina treated with calcium-antagonists in order to: define its usefulness in the evaluation of the short-term effectiveness of calcium-antagonist treatment; compare the results of the test with those of Holter monitoring; verify if the results of the test during the acute phase are correlated with the long-term response to treatment. In all patients a control period lasting 2-6 days was carried out, after which a treatment period with calcium-antagonists (nifedipine, diltiazem, verapamil), lasting 2-8 days, was instituted. In 20 patients only 1 calcium-antagonist was evaluated, in 1 patient 2 calcium-antagonists and in 4 all of them. Scalar ergonovine test was carried out in control conditions and repeated during each calcium-antagonist treatment period. During both control and treatment periods all patients underwent Holter monitoring for evaluation of frequency of the spontaneous attacks. After the acute phase 21 of the 25 patients were discharged on calcium-antagonist treatment and followed-up for a mean period of 11 +/- 7 months. In control conditions ergonovine test was positive in 24 patients at a mean dose of 0.11 +/- 0.09 mg.(ABSTRACT TRUNCATED AT 250 WORDS)

To verify whether beta-endorphin plasma levels influence the presence of anginal symptoms, 74 consecutive male patients were studied. All patients had previously documented coronary artery disease and reproducible exercise-induced myocardial ischemia. Thirty-five patients (Group I) had a history of angina and reported anginal symptoms during exercise stress testing; 39 patients (Group II) were asymptomatic and had documented silent myocardial ischemia during exercise. Baseline beta-endorphin plasma levels were measured in blood samples taken before exercise stress testing and analyzed by beta-endorphin-I125-RIA Kit-NEN (a radioimmunoassay method). The mean baseline beta-endorphin plasma level was 22.5 +/- 19 pg/ml in patients with anginal symptoms compared with 43.7 +/- 28 pg/ml in asymptomatic patients (p less than 0.001). Baseline blood pressure and heart rate-systolic pressure (rate-pressure) product at baseline and at ischemia threshold (1 mm ST segment depression) were similar in the two groups. Group II patients had a longer exercise duration (p less than 0.01), more pronounced ST segment depression (p less than 0.001) and a higher peak rate-pressure product (p less than 0.01). The extent of coronary artery disease, ejection fraction and left ventricular end-diastolic pressure were similar in the two groups. These data suggest that higher baseline beta-endorphin plasma levels may play a role in the decreased sensitivity to pain in patients with silent myocardial ischemia. In addition, different beta-endorphin levels can be associated with a different sensitivity to pain.