Steven Wolfson

Lyme Carditis: Cardiac Abnormalities of Lyme Disease

We studied 20 patients, mostly young adult men, with cardiac involvement of Lyme disease. The commonest abnormality (18 patients) was fluctuating degrees of atrioventricular block; eight of them developed complete heart block. Thirteen patients had evidence of more diffuse cardiac involvement: electrocardiographic changes compatible with acute myopericarditis (11 patients), radionuclide evidence of mild left ventricular dysfunction (five of 12 patients tested), or frank cardiomegaly (one patient). Heart involvement was usually preceded by erythema chronicum migrans and sometimes accompanied by meningoencephalitis, facial palsy, arthritis, elevated serum IgM levels, or cryoglobulins containing IgM. The duration of cardiac involvement was usually brief (3 days to 6 weeks). The clinical picture in these patients has similarities to acute rheumatic fever; but in Lyme disease, complete heart block may be commoner, myopericardial involvement tends to be milder, and valves seem not to be affected.

Propranolol and angina pectoris

Abstract Propranolol may offer an approach to the treatment of anginal pain which is refractory to conventional modes of therapy. Its efficacy may result from (1) lowering both left ventricular mechanical and metabolic requirements, (2) interference with sensory perception of anginal pain, or (3) blockade of adrenergic coronary vasoconstrictor activity which may precipitate angina in some subjects. Neither clinical nor resting physiologic data seem to be of value in predicting the response of a given patient to the drug.

Regional cardiac prostaglandin release during myocardial ischemia in anesthetized dogs.

Cardiac prostaglandin release was studied in closed-chest dogs during acute coronary occlusion. Aortic and coronary sinus blood was obtained before, and at intervals after, balloon occlusion of the left anterior descending artery in seven dogs. Samples were assayed for prostaglandins F, E, and A by radioim-munoassay. All dogs demonstrated prostaglandin F release. Mean ± se postocclusion aortic levels were 0.26 ± 0.01 ng /ml; coronary sinus levels were 0.67 ± 0.01 ng/ml [P < 0.001). In six dogs, prostaglandin E also was released. Mean postocclusion aortic levels were 0.24 ± 0.01 ng/ml; coronary sinus, 0.44 ± 0.01 ng/ml (P < 0.001). There was no release of prostaglandin A. To examine the site of prostaglandin release, simultaneous samples from the aorta, the coronary sinus, and the great cardiac vein were obtained before and after left circumflex artery occlusion in six additional studies. The great cardiac vein drained effluent from nonischemic myocardium, whereas the coronary sinus drainage included blood from both ischemic and nonischemic zones. All six dogs demonstrated prostaglandin F release from the ischemic region. Mean postocclusion aortic prostaglandin F was 0.32 ± 0.01 ng/ml. Coronary sinus prostaglandin F was 1.69 ± 0.03 ng/ml (P < 0.001), whereas the great cardiac vein level remained at 0.34 ± 0.01 ng/ml (P > 0.05). Prostaglandin E was released from both ischemic and nonischemic regions. Mean aortic prostaglandin E was 0.21 ± 0.01 ng/ml; great cardiac vein, 0.55 ± 0.02 ng/ml (P < 0.001); and coronary sinus, 1.07 ± 0.04 ng/ml (P < 0.001). These results have led us to conclude that the different local availability of prostaglandins E and F may influence the cardiac response to ischemia.

Cardiac prostaglandin release during myocardial ischemia induced by atrial pacing in patients with coronary artery disease

The relation between myocardial release of prostaglandin and myocardial ischemia was studied in 12 selected patients with multivessel coronary artery disease. These 12 were chosen for analysis because they experienced angina pectoris, ischemic electrocardiographic changes and decreased myocardial lactate uptake during atrial pacing. Simultaneous aortic and coronary sinus blood samples were obtained at rest, during angina and after recovery and were assayed for prostaglandins F, E and A with radioimmunoassay. Cardiac release of prostaglandin F was observed during angina in 11 of 12 patients. Aortic prostaglandin levels remained constant throught each study. During angina, the mean aortovenous difference (+/- standard error) was -0.30 +/- 0.04 ng/ml (P less than 0.001) for prostaglandin F and -0.10 +/- 0.03 ng/ml (Pless than 0.001) for prostaglandin E. There was no significant release of prostaglandin A. Blood samples were also drawn at subanginal heart rates in two patients. Prostaglandin F was released only during angina. In three control patients with a chest pain syndrome and normal coronary arteries, comparable atrial pacing produced no release of prostaglandin F, E or A. These results, together with the known vascular and metabolic actions of prostaglandins, suggest that these pharmacologically active compounds may also play a physiologic role in the cardiac response to ischemia in man.

Life-threatening ventricular arrhythmias induced by exercise. Cessation after coronary bypass surgery.

In three patients with clinical ischemic heart disease ventricular tachycardia developed during standard exercise testing. Despite suppressive antiarrhythmic therapy, ventricular tachycardia during exercise persisted in one patient; ventricular fibrillation requiring cardiopulmonary resuscitation developed in the other two. Coronary angiography revealed significant obstructive coronary artery disease with no ventricular aneurysm in all three patients. Aortocoronary saphenous vein bypass surgery was performed successfully without electrocardiographic or clinical evidence of intraoperative myocardial infarction. Postoperative cineangiography documented graft patency, and repeated exercise testing failed to elicit any ventricular irritability in these patients. They have remained asymptomatic with no antiarrhythmic therapy for up to 2 years postoperatively.

Alcohol-induced prinzmetal variant angina

Prinzmetal variant angina occurred in a 47 year old man only in association with the ingestion of alcohol. Results of exercise testing were normal. Coronary arteriography substantiated the presence of two significant coronary lesions. Double aortocoronary saphenous vein bypass grafts resulted in complete relief of symptoms.

Retrograde left ventricular catheterization in patients with an aortic valve prosthesis.

Twenty-seven consecutive patients with an aortic valve prosthesis were evaluated with retrograde left ventricular catheterization. The prosthesis was successfully crossed, permitting hemodynamic and angiographic evaluation of function of the prosthetic valve, left ventricle and mitral valve in all 27 cases. No complications were encountered. In patients with active endocarditis or recent embolization, the retrograde technique was avoided when possible, and attempts were made to utilize other techniques for study. However, three such patients were evaluated with the retrograde technique without complication. Examination of pressure tracings and cineangiographic films suggested only minor interference with valve poppet movement induced by the catheter transversing the valve. In three cases, hemodynamic data were recorded with the catheter crossing the prosthesis at one time and a paraprosthetic valve defect at another time. Identical gradients were recorded. This series documents the safety and efficacy of the retrograde approach, which is proposed as an alternative to the transseptal technique and left ventricular puncture.

Epinephrine Infusion in Man Standardization, Normal Response, and Abnormal Response in Idiopathic Hypertrophic Subaortic Stenosis

A standard test was designed for measurement of the effect of epinephrine infusion on systolic time intervals in 14 normal subjects as a dose-response phenomenon. In order that we might examine the sensitivity of the test, it was applied in nine patients with idiopathic hypertrophic subaortic stenosis.Normal subjects had a characteristic response—a progressive shortening of the duration of electromechanical systole, left ventricular ejection time, and pre-ejection period. Their left ventricular ejection time, corrected for heart rate, did not change. Patients with idiopathic hypertrophic subaortic stenosis responded to epinephrine infusion with paradoxical lengthening of their left ventricular ejection time, corrected for heart rate. After beta blockade (with propranolol), reinfusion of epinephrine shortened the left ventricular ejection time, corrected for heart rate, to normal levels.

Risk of death related to coronary arteriography: Role of left coronary arterial lesions

Seven deaths occurred within 5 days after study in 800 consecutive patients undergoing arteriography. All seven patients had severe anginal symptoms at rest or with minimal exertion, and all had extensive coronary artery disease. Four had left main coronary artery disease, and three had hemodynamically equivalent lesions involving both the proximal left anterior descending and circumflex branches. It is postulated that these deaths are due to a stress imposed upon patients in unstable condition with a particularly extensive myocardial perfusion deficit.

Effect of Therapy on Survival in Angina Pectoris.

Excerpt The prognosis of patients treated with either propranolol, internal mammary artery implantation (IMI), or conventional therapy for angina pectoris was compared. Forty-three patients were tr...