Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion.

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical failure of streptokinase due to an unsuspected high titer of antistreptokinase antibody.

Neutralization of streptokinase by an unsuspected high titer of antistreptokinase antibody prevented activation of the fibrinolytic system and induction of a lytic state in a 62 year old man with an acute inferior myocardial infarction. There was no decrease in serum fibrinogen, minimal decrease in serum plasminogen and only a small increase in serum fibrin degradation products after intravenous administration of 1.5 million units of streptokinase. A high titer of antistreptokinase antibody, sufficient to neutralize 1.5 million units of streptokinase, was demonstrated by semiquantitative counterelectrophoresis . There was no clinical evidence of coronary artery reperfusion, and coronary angiography confirmed complete occlusion of the left circumflex artery.

Effects of late coronary artery reperfusion after myocardial necrosis is complete.

Early reperfusion salvages reversibly injured ischemic myocardium. Late reperfusion, after necrosis is complete, could be beneficial by accelerating healing, or the hemorrhage and contraction-band necrosis associated with reperfusion could impair healing. In closed-chest anesthetized dogs the left anterior descending coronary artery was occluded with a balloon-tipped catheter for either 1 day followed by reperfusion for 6 days (n = 9) or for 7 days without reperfusion (n = 9). All dogs were killed after 7 days. Pathologic changes were studied in transverse whole-mount ventricular histologic sections. When the two groups were compared, no differences were found in: (1) infarct size, 15.7 +/- 9.9% vs 10.2 +/- 8.6 (mean +/- SD); (2) number of transmural infarcts, 5 of 9 vs 6 of 9; (3) ratio of infarcted/normal wall thickness, 0.93 +/- 0.09 vs 0.95 +/- 0.13; (4) thickness of zone of collagen deposition at periphery of infarct, 1.69 +/- 1.16 mm vs 1.67 +/- 0.56; and (5) amount of hemorrhage, calcification, and inflammation. Thus, in this model, reperfusion after necrosis is complete did not improve or impair healing.

ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction.

In 5 of 69 patients (7%) undergoing intracoronary or intravenous streptokinase treatment, the ST-segment elevations in leads V1 to V5 were caused by occlusion of the right rather than the left anterior descending coronary artery and by myocardial infarction (MI) of the right ventricular (RV) wall rather than the anterior left ventricular (LV) wall or the ventricular septum. RV involvement was documented by technetium pyrophosphate uptake, hypokinesia, dilatation and depressed RV ejection fraction. The left anterior descending artery was patent and the anterior LV wall had normal thallium-201 uptake, no technetium uptake and normal wall motion. ST-segment elevation was highest in lead V1 or V2 and decreased toward lead V5; in patients with anterior LV MI, the ST-segment elevations are usually lowest in lead V1 and increase toward the V5 lead. In contrast to anterior LV infarcts, the R waves in leads V1 to V5 did not decrease and Q waves did not evolve with progression of the MI. The ST-segment elevations in leads V1 to V5 in our patients were associated with small or absent ST-segment elevations in leads, II, III and aVF, suggesting that in other cases of RV infarction, the appearance of ST-segment elevations in leads V1 to V5 is blocked by the dominant electrical forces of the LV inferior MI. This suggestion was confirmed in a canine model. Recognition of the presence of RV infarction may be therapeutically important.

Intermittent brief periods of ischemia have a cumulative effect and may cause myocardial necrosis.

We investigated the effects of brief intermittent periods of ischemia on myocardial viability. Brief periodic coronary occlusions were produced up to 18 times by inflating and deflating the balloon of an intracoronary No. 2F catheter for periods of 15, 10 or 5 minutes, followed by 15-minute periods of reperfusion. Creatine kinase (CK) release, triphenyl tetrazolium chloride staining, and light and electron microscopy were used to detect the presence of myocardial necrosis. For the study of CK release, blood was taken from the great cardiac vein and the aorta before and at 5-minute intervals during each left anterior descending coronary occlusion, as well as during and 1, 5, 10 and 15 minutes after balloon deflation. In seven of 24 dogs with 15-minute occlusions, in five of 21 dogs with 10-minute occlusions, and in three of 32 dogs with 5-minute occlusions, small but distinct areas of subendocardial necrosis were present. In all dogs with morphologic proof of necrosis, there was periodic release of CK into the great cardiac vein, which peaked immediately after reperfusion, reflecting CK washout. Thus, brief periods of ischemia, which when single do not cause necrosis, have a cumulative effect and may cause myocardial necrosis. This mechanism of necrosis may be relevant clinically in patients with frequent anginal episodes. Since many dogs of this study did not have any myocardial necrosis, the findings also suggest that intermittent reperfusion has a beneficial effect and may prevent necrosis, even when total occlusion time exceeds 200 minutes.

Echocardiography and valve replacement in the critically ill patient with acute rheumatic carditis.

In 4 critically ill patients with acute rheumatic carditis, valve incompetence, and severe life-threatening cardiac failure, medical treatment consisting of bedrest, oxygen, digitalis, diuretics, and steroids produced little or no clinical improvement. Echocardiography showed that in each patient myocardial function was relatively well preserved despite active rheumatic carditis and the critical clinical state. Emergency valve replacement was performed, and a good clinical result was achieved in all 4 patients.

Echocardiographic left ventricular function in mitral stenosis.

Left ventricular function was measured by echocardiography in 22 patients with pure mitral stenosis. Thirteen patients underwent closed transventricular mitral valvulotomy and nine underwent open mitral valvulotomy using cardiopulmonary bypass. Preoperative left ventricular function was normal in most patients but was depressed in older subjects (P less than 0.05) and in those undergoing a second operation on the mitral valve (P less than 0.001). The decrease in left ventricular function was probably related to the duration of mitral valve disease, with fibrosis and rigidity of the subvalvar apparatus and posterobasal left ventricular wall. There was no change in ventricular dimensions or in left ventricular function as measured by percentage shortening of the left ventricular diameter and ejection fraction 7 to 12 days after open or closed mitral valvulotomy.

Echocardiographic left ventricular function in aortic and mitral incompetence and the effect of valve replacement.

Left ventricular (LV) function was studied by echocardiography in 28 patients with volume overload of the LV before and after valve replacement. Of the 28 subjects, 19 had mitral valve disease (eight with mitral incompetence and 11 with mitral incompetence and stenosis) and nine patients had aortic incompetence. Patients with chronic mitral and aortic incompetence had marked LV enlargement with normal or slightly depressed systolic function; in those with acute mitral incompetence the degree of cardiomegaly was less and the state of LV function depended on the underlying cause of valvular incompetence. Valve replacement was followed by a decrease in LV end-diastolic volume and this occurred in the first week after operation. There was a gradual improvement in LV function in some patients, as measured by normalized mean velocity of posterior LV wall motion. Paradoxical septal motion occurred in many patients after operation but improved in the late postoperative period.