Usefulness of systolic time intervals in coronary artery disease.

This review summarizes current knowledge concerning the value of systolic time intervals in coronary artery disease. Although the usual pattern of prolongation of the preejection period (PEP) and shortening of the left ventricular ejection time (LVET) characteristic of left ventricular failure is seen in acute myocardial infarction, the systolic time intervals (as well as all other measures) are profoundly influenced by adrenergic hyperactivity characteristics of this disorder. Adrenergic stimulation normally shortens both the PEP and LVET indexes and decreases the PEP/LVET ratio. The degree of shortening of electromechanical systole (QS2) is directed related to the excessive adrenergic tone. Patients with the greatest systolic time interval abnormalities have a poorer prognosis, a greater incidence of congestive heart failure and more abnormalities of directly measured indexes of left ventricular performance. The systolic time intervals are useful for assessing left ventricular performance in chronic coronary artery disease as well. In chronic coronary artery disease the PEP/LVET ratio and angiographically determined left ventricular ejection fraction are closely correlated ( r = -0.76), but the level of this correlation is less than that in other forms of left ventricular disease. The left ventricular ejection time index is prolonged after exercise in patients with angina pectoris when compared with findings in normal subjects. Failure of the ischemic ventricle to respond to adrenergic stimulation is the most likely mechanism. Addition of the postexercise left ventricular ejection time to standard treadmill stress testing identifies a significant number of patients (23 percent) who would have had false negative results by electrocardiographic criteria alone. In addition, this index provides confirmatory evidence in those with apparently positive electrocardiographic test data. The systolic time intervals have been useful in assessing both medical and surgical therapy in coronary artery disease. The test can be performed repeatedly and provides a measure of both left ventricular performance and extent of adrenergic hyperactivity. Thus, evaluation of therapy represents the most useful future application of systolic time intervals.

Noninvasive myocardial imaging with potassium-43 and rubidium-81 in patients with left bundle branch block.

Noninvasive myocardial imaging with potassium-43 and rubidium-81 has been used successfully to identify areas of infarction and exercise-induced ischemia as regions of decreased radioactivity. The image defects observed are believed to be due to a decreased radionuclide uptake in regions of myocardial scar or to heterogeneous myocardial accumulation of tracer as a result of regional ischemia. Of 27 patients with left bundle branch block studied with noninvasive imaging at rest and during exercise, 25 manifested at rest reduced radioactivity in the region of the interventricular septum. This pattern is similar to that seen in patients with anteroseptal myocardial infarction. Sixteen of the 27 patients underwent diagnostic coronary arteriography and left ventriculography. Only five of these patients had evidence of either previous infarction or significant obstructive coronary artery disease as assessed with clinical or angiographic criteria, or both. Although the image defect was routinely demonstrated at rest in patients with left bundle branch block, this defect was generally normalized or less distinct with exercise in patients with no anatomic heart disease. In contrast, a larger, more distinct or new image defect with exercise correctly identified the presence of significant obstructive coronary artery disease in patients with left bundle branch block. In the clinical application of noninvasive myocardial imaging, these image defects observed at rest can lead to the false pasitive radionuclide interpretation of anteroseptal myocardial infarction.

Negative inotropic effect of lidocaine in patients with coronary arterial disease and normal subjects.

The effect of administration of lidocaine on left ventricular performance was studied using systolic time intervals in nine normal subjects, eight patients with stable angina, and 15 patients with acute myocardial infarction. The greatest response in systolic time intervals occurred at three minutes after intravenous injection of lidocaine (100 mg), with values returning to baseline at 10 to 15 minutes. Administration of lidocaine produced a significant prolongation of the preejection period (PEP) corrected for heart rate in all groups and a prolongation of the ratio of PEP to left ventricular ejection time (PEP/LVET) in patients with angina. The group with acute myocardial infarction exhibited a hyperadrenergic state, as shown by a short baseline QS2I. The QS I was lengthened by administration of lidocaine in all groups, but this was more profound in those with acute myocardial infarction. These changes in systolic time intervals were still present at two hours after injection in six patients with acute myocardial infarction in whom an infusion of lidocaine followed the initial bolus. The effect of administering lidocaine after intravenous injection of propranolol (5 mg) was also studied in six normal subjects. Although propranolol therapy along prolonged the PEP/LVET, a further significant prolongation followed subsequent injection of lidocaine.

Abnormal left ventricular wall motion at mid-ejection in patients with coronary heart disease.

The degree of inward motion at mid-ejection was examined for seven segments on the silhouettes of left ventriculograms taken in the 30 degrees RAO projection in patients with normal coronary arteries. The pattern of wall motion described in these patients was used to distinguish abnormalities in mid-systolic wall motion. One or more abnormally contracting segments were found at mid-ejection of 27 of 42 patients with obstructive coronary artery disease and normal end-systolic wall motion. Of the 57 segments found in these patients, 41 or 72% corresponded to sites of significant coronary artery obstruction. Seven patients had electrocardiographic evidence of prior infarction. Following coronary graft surgery in eight patients improved motion was found in association with graft patency in seven priviously delayed segments and two new areas of delayed wall motion associated with nonpatent grafts and electrocardiographic changes of infarction appeared. We postulate that some of the myocardial fibers in late contracting segments have been injured or infarcted and are able to contract effectively only during the latter half of ejection when ventricular wall tension is reduced.

Clinical correlates of coronary cineangiography in young males with myocardial infarction.

Thirty-eight men who suffered acute transmural myocardial infarction before age 40, and after recovery were New York Heart Association functional Class I or II, were studied by noninvasive means and by coronary angiography in order to determine whether these nonivasive studies could predict the presence of significant coronary artery disease remote from that felt to be responsible for the previous myocardial infarction. Patients were divided into two groups on the basis of the absence (Group I) or presence (Group II) of obstructive disease in a major coronary artery supplying myocardium remote from the prior myocardial infarction. There were 21 patients in Group I and 17 patients in Group II. They did not differ with respect to age, abnormalities of lipid or glucose metabolism, family history, history of hypertension or cigarette use, presence of obesity, or infarct localization. Ten of 17 patients in Group II had angina pectoris; only 3/21 patients in Group I had angina pectoris (p less than 0.01). All 12 patients tested in Group II had a positive maximal exercise tolerance test; only 1/17 patients tested in Group I was similarly positive (p less than 0.001). The absence of angina pectoris and the presence of a negative maximal exercise tolerance test is strong evidence against the pressure of significant CAD remote from that responsible for the prior myocardial infarction.