Idiopathic ventricular tachycardia. An intracardiac electrical, hemodynamic and angiographic assessment of six patients.

Six patients with idiopathic paroxysmal ventricular tachycardia were investigated by external electrocardiography, intracardiac electrography and pacing, exercise testing, cardiac catheterization and coronary angiography. All had normal hemodynamics and coronary arteries. His bundle electrography proved ventricular origin in five; one had no paroxysmal ventricular tachycardia during His bundle electrography. Treatment with diphenylhydantoin, 4.2 to 8.0 mg/kg/day, and propranolol, 0.8 to 2.7 mg/kg/day, appeared effective, well tolerated therapy in three, and procainamide and propranolol in one requiring medical treatment. Abstinence from tobacco and coffee abolished paroxysmal ventricular tachycardia in one of two who required no medication. The other has no recurrence of paroxysmal ventricular tachycardia since study.

Resection of acute posterior ventricular aneurysm with repair of ventricular septal defect after acute myocardial infarction.

Three patients with true posterior myocardial infarctions and ventricular septal defects were treated by posterior infarctectomy, closure of the defect, and appropriate combinations of mitral valve replacement and coronary grafting. Aortic balloon pumping was not used. The technique of infarctectomy and ventricular septal defect closure is illustrated. Two of the 3 patients have excellent long-term results.

Surgical correction of anomalous left coronary artery from the anterior sinus of valsalva.

Origination of the left main coronary artery from the anterior sinus of Valsalva is a rare congenital anomaly that has been associated with sudden death. Anatomical correction of this defect has only rarely been performed by unroofing the intramural segment of the proximal coronary artery or by widening the narrowed angulated origin of this anomalous vessel. This report describes the clinical course of a 33-year-old woman with this anomaly who experienced episodes of chest tightness associated with ischemic electrocardiographic changes. Surgical correction was performed by enlarging the ostium of the anomalous artery with a "sphincteroplasty" technique. Thallium scanning, which was positive prior to surgery, was normal postoperatively. The patient remains asymptomatic 6 months after surgical correction.

Multiple cardiovascular injuries and motor vehicle accidents.

A patient sustained blunt chest trauma in a motor vehicle accident. Cardiovascular trauma was initially obscured by more obvious orthopedic injuries. Thoracic aortic transection with false aneurysm formation was discovered incidentally during cardiac catheterization for traumatic tricuspid insufficiency. Successful repair of both lesions was subseqeuntly performed. This case demonstrates the difficulty in recognizing cardiovascular trauma in survivors of motor vehicle accidents and emphasizes the need for an aggressive diagnostic approach with consideration of coexisting injuries in patients who have sustained blunt chest trauma.

Traumatic left ventricular aneurysm. Two cases with normal coronary angiograms.

Two young males had traumatic left ventricular aneurysm and normal coronary angiograms. Trauma was penetrating (bullet) in one and nonpenetrating (fist blow) in the other. Recurrent ventricular tachycardia in one and a systemic embolus in the other required aneurysmectomy. The patients are free of symptoms 42 and 21 months after surgery. The presence of traumatic ventricular aneurysm and normal coronary angiograms suggests that myocardial necrosis following chest trauma is often caused by direct injury to the myocardium rather than by injury to occlusion of the coronary arteries. Therefore, coronary artery bypass surgery may be unnecessary or even hazardous in persons with chest trauma and evidence of early myocardial necrosis.

The angiotensin infusion test as a method of evaluating left ventricular function.

Fifteen patients had left ventricular function measured by the angiotensin infusion method. Seven patients had no evidence of heart disease, and eight patients had angina pectoris and coronary arteriographic evidence of coronary disease without congestive heart failure. During angiotensin infusion, those patients without heart disease had a decrease in cardiac index (average, 0.63 L. per minute per square meter) and a decrease in heart rate (average, 12 beats per minute.) The ventricular function curve had a poor SWI response in four of the seven subjects. The patients with coronary artery disease also had a reduction in cardiac index during angiotensin (average, 0.44 L. per minute per square meter) and the heart rate was unchanged in four subjects, increased in two subjects, and decreased in two subjects. Six of the subjects had flat or descending slopes on the function curve, and in one subject there was only a very gradual ascending slope. Many of the curves of both groups looked similar so that the function curves did not differentiate between those patients with or without heart disease. The mechanism for production of bradycardia, reduction of cardiac output, and depressed function curves with angiotensin is multifactorial, but is probably due to the baroreceptor reflex response, the increase in coronary artery resistance, and possible to the direct effect of increased left ventricular afterload itself. The ventricular response to angiotensin is so variable that the angiotensin infusion method of evaluating ventricular function is not reliable.