Follow-up catheterization of patients with myocardial infarction during coronary artery bypass surgery.

Of 197 consecutive patients having aortocoronary bypass grafts over a 30 month period, 38 (19 per cent) had ECG evidence of myocardial infarction. The infarctions occurred more commonly in patients receiving multiple grafts. The infarctions were usually in areas supplied by grafted vessels. The infarctions occurred most often in the inferior wall, even when multiple vessels were grafted. Eleven patients with intraoperative infarction have had repeat postoperative coronary arteriograms. Seven had all grafts patent; three of these patients had hypokinesis of the infarcted wall. Four of the 11 patients had one or more occluded grafts; three of these patients had an area of hypokinesis. We conclude that intraoperative myocardial infarction is a common problem in aortocoronary bypass surgery and is not necessarily caused by graft occlusion.     

Percutaneous transluminal coronary angioplasty in acute myocardial infarction

Percutaneous transluminal coronary angioplasty (PTCA) has, in general, been restricted to therapy for patients with angina pectoris. Thrombolytic therapy and guide wire recanalization have been used to recanalize coronary arteries in patients with evolving myocardial infarction. Recently we and others have examined the use of PTCA to recanalize the acutely occluded artery associated with the early evolving phase of myocardial infarction. PTCA was performed as definitive therapy in eight patients with acute myocardial infarction. Seven of these had totally occluded arteries to the region of infarct. The infarct-related artery was open within 20 minutes in each of these cases. PTCA recanalization resulted in evidence for reperfusion in each case. Residual stenoses either were not present or were minimal. The procedure was well tolerated. These preliminary results suggest that PTCA may be a reasonable alternative to intracoronary thrombolytic therapy in certain patients with acute evolving myocardial infarction.     

Sinus and A-V nodal dysfunction following myocardial infarction.

A patient in whom syncopal episodes occurred following an inferior myocardial infarction is described. Electrocardiographic monitoring revealed periods of profound sinus bradycardia and AV block during syncope. In addition, transient spontaneous prolongations of the PR interval due to AV nodal delay and episodes of atrial fibrillation also occurred. Sinus node recovery time following atrial overdrive was within normal limits. Symptoms disappeared following the insertion of a permanent, demand pacemaker. The onset of symptoms following myocardial infarction suggests that dysfunction of the sino-atrial and AV nodes may have been the result of ischemic damage during the infarction.     

Ferrokinetic studies in acute myocardial infarction.

Serum iron levels were determined in 16 patients with AMI at different days following the event and in five patients either treated with steroids or suffering from diseases acting as stress factors. Patients with AMI showed a marked decrease in serum iron concentrations, the lowest value being recorded at day 3 after the event; serum iron returned to normal level at day 12. These alterations in iron concentration were not accompanied by changes in the 24 hour urine excretion of iron. On the other hand, a significant shortening of the half-time 59Fe plasma clearance and an early increase in 59Fe incorporation into the red blood cells were found immediately after the event. These values returned to normal in all but one patient, who had in addition polycythemia. In the five patients comprising the control group, serum iron, iron excretion in urine, and ferrokinetics were within the normal limits at all times. Since in AMI patients the 11-OHCS values were found to be significantly higher on the day following the infarction than on day 15 after the event, it is suggested that the decrease in iron concentration in these patients may be connected with changes in plasma 11-OHCS levels.     

Perioperative myocardial infarction related to coronary bypass surgery.

Frank lead electrocardiograms were recorded from 149 normal and abnormal adult males using four different electrode placements. All chest electrodes were placed at: (1) the fourth intercostal space level, (2) the fifth intercostal space level, (3) the fourth intercostal space level with V₄ substituted for C, and (4) the fifth intercostal space level with V₄ substituted for C.Differences in mean values of many commonly used amplitudes and orientations were not statistically significant among the four recording methods, but amplitude differences for individual subjects were often large and difficult to predict. When V₄ is substituted for C, as commonly done in some laboratories, R_x decreased and R_z increased by more than 10 per cent in about 40 per cent of the cases. In about 70 per cent of the cases, R_x and R_z changed significantly when electrode level was shifted from the fifth to the fourth intercostal space. For these 70 per cent, it does not appear possible to accurately predict increase or decrease of R_x, R_z, or QRS_m.Analysis programs which depend on individual amplitude measurements are likely to be significantly affected by electrode placement. It is suggested that criteria for analysis programs developed using a specified version of the Frank system should ideally be applied only to electrocardiograms recorded in the same manner.     

Electrocardiographic changes simulating acute myocardial infarction caused by hyperkalemia: report of a patient with normal coronary arteriograms.

A patient is described with severe diabetic ketoacidosis and hyperkalemia who presented with an ECG resembling an acute anterior wall myocardial infarction. Treatment of hyperkalemia resulted in prompt return of the ECG towards normal. Subsequent work-up including exercise testing and selective coronary arteriography ruled out any significant coronary artery disease suggesting that the ECG changes were probably caused by hyperkalemia. While similar changes have rarely been described in the past, this would appear to be the first such case in whom coronary artery disease was ruled out by a negative exercise testing and coronary arteriography.     

Intracoronary thrombolysis in evolving myocardial infarction

After experimental studies in dogs confirmed the feasibility and safety of rapid intracoronary thrombolysis by local infusion of Thrombolysin (streptokinase and plasmin), intracoronary thrombolysis was attempted in 20 patients with evolving myocardial infarction who were hospitalized within 3 hours from the onset of symptoms during the day and within 2 hours at night. Thrombolysin was infused in the immediate vicinity of the site of coronary occlusion using a 0.85 mm outer diameter catheter advanced through the lumen of the Judkins catheter. Reperfusion was achieved in four patients after an average of 43 minutes of Thrombolysin infusion at a rate of 2000 IU/min and in 15 patients after an average of 21 minutes of Thrombolysin infusion at a rate of 4000 IU/min. The failure to open the artery in one patient may have been caused by our inability to advance the infusion catheter close to the site of occlusion. Rethrombosis occurred in one patient 8 days after reperfusion and 2 days after discontinuation of anticoagulants because of a history of chronic alcoholism. Wall motion and perfusion studies showed improvement following reperfjsion. Patency of the artery was achieved an average of 4 hours after the onset of symptoms. The need for earlier reperfusion is emphasized.     

The significance of fever in acute myocardial infarction: A reappraisal

A reappraisal of the significance of fever in acute myocardial infarction was undertaken in the controlled environment of a coronary-care unit. With the use of standardized criteria, 334 patients were given a diagnosis of acute myocardial infarction. The seven-day point prevalence for fever was 65.3 per cent, with a maximal incidence of 72 per cent on the second day. No significant correlation could be found between maximal temperature levels, degree of enzyme elevation, and leukocyte count. A policy of making cultures from those patients with fever identified infection in 63 (18.9 per cent) with a high correlation in this group with heart failure, atelectasis, and the use of urinary and central venous pressure catheters. High fever or fever beyond the fourth day of illness was most likely caused by respiratory or urinary tract infection, frequently related to gram-negative organisms. These data reinforce the commonness of fever but also indicate that the prevention, recognition, and treatment of infections should be an important part of the management of patients with acute myocardial infarction.     

Tritiated digoxin. XX. Tissue distribution in experimental myocardial infarction

The role and potential hazards of digitalis glycoside administration in acute myocardial infarction remain controversial. We investigated the concentration of tritiated digoxin in normal, ischemic, and infarcted left ventricular myocardium of the dog after ligation of the anterior interventricular coronary artery. The normal homogeneous distribution of tritiated digoxin in the normal canine left ventricle was altered following acute myocardial infarction. The ischemic and infarcted zones exhibited a marked diminution in digoxin concentration. Oxidative phosphorylation determinations confirmed tissue hypoxia in the infarcted zone. The gradient of digoxin concentration between normal, ischemic, and infarcted zones of myocardium may potentiate the development of an arrhythmia in the electrically unstable infarcted myocardium.     

High mortality early reinfarction with first nontransmural myocardial infarction

Thirty-eight patients with first nontransmural myocardial infarction were studied to determine prognosis and clinical markers of a high-risk subgroup. We found a high incidence of reinfarction (18%) at a median time of 16 days post nontransmural infarction (seven patients). Reinfarction was uniformly associated with death within 24 hours. A total of 14 patients (37%) either died (eight patients) or required urgent revascularization (six patients). Predominant ST segment depression with presenting nontransmural infarction and a history of prior angina were associated with increased mortality (p less than 0.05 and p = 0.05, respectively). We conclude that patients with nontransmural infarction are at high risk for early recurrent infarction. Patients with history of prior angina and predominant ST segment depression may be at particularly high risk. Reinfarction in these patients is frequently extensive. We recommend that these patients be considered for early coronary angiography.     

Abnormal mitral valve motion associated with ventricular septal defect following acute myocardial infarction.

It is often difficult to make the clinical distinction between acute mitral regurgitation caused by papillary muscle dysfunction or rupture and ventricular septal defect complicating an acute myocardial infarction. A case of a patient with rapidly progressive congestive heart failure and a loud murmur is presented. Echocardiography strongly suggested the presence of a flail posterior mitral leaflet. However, the patient was subsequently found to have rupture of the interventricular septum. This diagnosis was made with bedside right heart catheterization and was later confirmed by left ventriculography and direct inspection at the time of surgery. The mitral valve apparatus was completely normal. Thus this case demonstrates the apparent lack of specificity of the accepted echocardiographic criteria for flail mitral leaflet and acutely ruptured interventricular septum, and the potential necessity of cardiac catheterization to distinguish between these entities.     

Regional myocardial perfusion at rest and during intracoronary papaverine in patients with coronary artery disease

Regional myocardial perfusion was measured in 32 patients with the xenon-133 washout technique at rest and after 5 mg of intracoronary papaverine. Areas of decreased perfusion and/or decreased vasodilation were identified visually from computer-generated functional images. The locations of arteries and stenoses, obtained from identically positioned cineangiograms, were overlaid on the functional images. Perfusion rates for 62 myocardial regions were calculated and correlated with the percentage of stenosis. There was no association between degree of stenosis and perfusion at rest. Regional myocardial perfusion increased after papaverine in regions supplied by coronary arteries without stenoses (0% to 25%), 88.6 ± 4.7 ml/min/100 gm. This increase was significantly greater (p < 0.001) than the increase in regions supplied by 51% to 75% stenoses (23.7 ± 6.3 ml/min/100 gm), or 76% to 99% stenoses (12.9 ± 6.3 ml/min/100 gm), or 100% stenoses (2.5 ± 3.8 ml/min/100 gm). Thus there was an inverse relationship between the increase in myocardial perfusion stimulated by papaverine and the degree of coronary artery stenosis measured angiographically. In regions supplied by two stenoses in series, vasodilation produced less of an increase than a single stenosis of a similar degree.