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The ability to quantitate the amount of permanent left ventricular dysfunction in patients with unstable ischemic heart disease would have important clinical value. Left ventricular function curves were constructed in sixteen patients with acute myocardial infarctions and five patients with unstable angina pectoris syndrome at an average of 56 hours (+/- 8) after the onset of symptoms. Fifty ml increments of low molecular weight dextran were rapidly infused into the right antrium during constant monitoring of the pulmonary artery end-diastolic pressure (PAEDP) via a Swan-Ganz thermodilution catheter. An average of 400 ml (range 200-800) was infused to produce a significant change in the PAEDP (range 3-13 mm Hg). The cardiac index was measured before and after the dextran infusion. The slope of the left ventricular function curve was calculated by dividing the change in the cardiac index by the change in the PAEDP. The sixteen patients with acute myocardial infarction underwent left heart catheterization and left ventricular biplane angiography an average of six months later. The five patients with unstable angina pectoris were studied within one month. The slope value of the left ventricular function curve was compared angiographic ejection fraction by linear regression analysis and the correlation coefficient was 0.80. These data demonstrate 1) the slope of the left ventricular function curve in patients with acute myocardial infarction or unstable angina correlates well with the angiographically calculated ejection fraction; 2) as early as two days post myocardial infarction, the residual impairment of left ventricular function can be estimated.

To evaluate the relative thrombolytic efficacy and complications of intracoronary vs high-dose, short-term intravenous streptokinase infusion in patients with acute myocardial infarction, we performed baseline coronary arteriography and then randomly allocated 51 patients with acute myocardial infarction to receive either intracoronary (n = 25) or intravenous (n = 26) streptokinase. Patients getting the drug by the intracoronary route received 240,000 IU of streptokinase into the infarct-related artery over 1 hr, whereas those getting the drug by the intravenous route received either 500,000 IU of streptokinase over 15 min (n = 10) or 1 million IU of streptokinase over 45 min (n = 16). Angiographically observed thrombolysis occurred in 76% (19/25) of the patients receiving intracoronary streptokinase, in 10% (1/10) of the patients receiving 500,000 IU of streptokinase intravenously, and in 44% (7/16) of the patients receiving 1 million IU of streptokinase intravenously. Among patients in whom thrombolysis was observed, mean elapsed time from onset of streptokinase infusion until lysis was 31 +/- 18 min in patients receiving intracoronary streptokinase and 38 +/- 20 min in those receiving intravenous streptokinase (p = NS). Among patients in whom intravenous streptokinase "failed," intracoronary streptokinase in combination with intracoronary guidewire manipulation recanalized only 7% (1/15). Fibrinogen levels within 6 hr after streptokinase were significantly lower in the patients receiving intravenous streptokinase (39 +/- 17 mg/dl) than the levels in those receiving intracoronary streptokinase (88 +/- 70 mg/dl) (p less than .05) but were similar 24 hr after streptokinase in the two groups. Bleeding requiring transfusion occurred in one patient in each group. Thus, in this prospective randomized trial of intracoronary vs intravenous streptokinase, hemorrhagic complications were few, although both regimens produced a systemic lytic state. Although the thrombolytic efficacy of intracoronary streptokinase was superior to that of high-dose, short-term intravenous streptokinase, the higher-dose intravenous regimen (1 million IU over 45 min) achieved thrombolysis in a significant minority (44%) of patients and might be useful therapy for patients not having access to emergency catheterization.

Two hundred-three patients had -echnetium 99m (stannous) pyrophosphate myocardial scintigrams for the evaluation of chest pain and suspected acute myocardial infarction. In addition to routine imaging at 60--90 minutes after injection of the radio-pharmaceutical, the blood pool was imaged immediately in each patient for comparison with routine anterior, left anterior oblique, and left lateral views. Further delayed studies were obtained when residual blood pool activity was identified. Seventy patients had acute myocardial infarction by clinical, electrocardiographic, and enzymatic (CK-MB) criteria. Sixty-five of these 70 patients with acute infarction had positive myocardial scintigrams, with one technically unsatisfactory study. Only four of the 70 patients had negative scintigrams when imaged 18--72 hours after infarction in this study. Technically satisfactory scintigrams were recorded in 125 patients without evidence of infarction. Ninety-six had negative scintigrams at 60--90 minutes, while 19 patients (15%) had precordial activity at 60--90 minutes which was identical in distribution to early blood pool images and cleared with further delay. With these included, the true negative incidence was 92%. Ten of 125 patients had false positive scintigrams; two had recent cardioversion with resultant chest wall damage. The other eight patients had previous infarction 1 1/2 to 72 months earlier and had akinetic segments shown angiographically in the areas of the persistently positive scintigrams. Myocardial scintigraphy correlates well with the presence of other evidence of acute infarction, as well as with the absence of acute infarction when residual blood pool activity is identified. False positive scintigrams can occur following cardioversion and in patients with previous myocardial infarction and resultant ventricular wall motion abnormalities.

Although biplane right anterior oblique-left anterior oblique (RAO/LAO) quantitative left ventricular (LV) angiography is commonly performed, justification of LV volume calculation using the area length method (originally formulated from anteroposterior-lateral (AP/LAT) angiograms) has been limited. To assess whether RAO/LAO and AP/LAT LV volumes are similar when computed by the area length method formula, we performed biplane cine LV angiography in both RAO/LAO and AP/LAT projections in random sequence in 21 patients and four LV models of known volume. LV silhouettes were drawn independently by two trained observers. Calculated angiographic volume of the models correlated almost exactly with their true volume (r = 0.999), establishing the absolute accuracy of this system. Rotation of the LV models through 90 degrees of obliquity at 10 degree increments demonstrated a mean change from true volume of only -5.4 +/- 0.7% (p less than 0.001). In the patient studies, rotation to the 30 degree RAO/60 degree LAO position was associated with significant changes in magnitude of biplane areas and long axes, but area length volume estimates were unchanged. Excellent correlation was found between area length calculated AP/LAT and RAO/LAO volumes with r = 0.90, 0.97, and 0.91 for end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (EF), respectively. Furthermore, interobserver agreement in volume assessment was excellent, with r = 0.98, 0.99, and 0.94 between observers for EDV, ESV, and EF, respectively. Interobserver and inter-method variability for estimates of LV volume and EF ranged from 5--10%. We conclude that when using RAO/LAO LV angiography, volume calculation by the area length method is justified.

SUMMARY The usefulness of thallium-201 (Tl-201) exercise myocardial scintigraphy in identifying patients with multivessel coronary artery disease (MVCAD) and residual jeopardized myocardium after myocardial infarction (MI) was evaluated in 32 patients 3 weeks after MI. All patients underwent 1) limited multilead submaximal treadmill testing, 2) thallium-201 (TI) myocardial scintigraphy at end-exercise and at rest, and 3) coronary and left ventricular angiography. TI-201 perfusion defects were categorized as either reversible (ischemia) or irreversible (scar). The conventional exercise test was designated positive if there was ST depression 2 1 mm and/or angina. Jeopardized myocardium (JEP) was defined angiographically as a segment of myocardium with normal or hypokinetic wall motion supplied by a significantly stenotic major coronary artery. MVCAD was defined as two or more significantly stenotic coronary arteries. “Significant” coronary stenosis was categorized as either 50–69% diameter narrowing or 2 70% diameter narrowing, thereby yielding, respectively, two subgroups each of jeopardized myocardium (JEP-50 and JEP-70) and MVCAD (MV-S0 and MV-70). Clinical findings of angina, heart failure or ventricular arrhythmias during the late convalescent period after MI occurred in four of 10 patients (40%) with MV-50, five of 16 (31%) with MV-70, four of 10 (40%) with JEP-50 and five of 18 (28%) with JEP-70, and thus were insensitive for detecting MVCAD and JEP. Reversible ischemia and/or a positive conventional exercise test occurred in five of 10 patients (50%) with MV-50, 13 of 16 (81%) with MV-70, four of 10 (40%) with JEP-S0 and 15 of 18 (83%) with JEP-70. All eight patients with both TI-201 reversible ischemia and a positive conventional exercise test had JEP-70. In 30 of 31 patients (97%) with angiographic asynergy, TI-201 scar was detected. No complications were associated with exercise testing. Thus, 3 weeks after MI, Tl-201 exercise myocardial scintigraphy is a safe, useful, noninvasive tool for identifying patients with MVCAD and residual JEP and is much more reliable than clinical findings during convalescence after MI.

Debate exists over the most appropriate form of treatment for patients with unstable angina pectoris. This study examined 106 patients randomized at the University of Alabama in Birmingham as part of the National Cooperative Study Group and focuses on the phenomenon of patients who fail medical therapy and thus require late surgery, and the costs of therapy. Discriminant function analysis revealed that the significant predictors (p less than 0.01) of patients who would later require surgery were: total number of vessels diseased, angina severly, presence of congestive heart failure, hypertension, and number of years that the patient had had angina. By means of this analysis, 85% of the late surgery patients were correctly predicted. Late surgery patients averaged 2.4 diseased vessels vs 1.5 for persistent medical patients (p less than 0.01). Mean charges for the first 2 years in the study were $6,226 (SD $2,967) for persistent medical patients, $10,416 (SD $2,146) for surgery patients, and $20,059 (SD $10,748) for late surgery patients (p less than 0.001). These data indicate that surgery is clearly an expensive procedure; but that it is more expensive for late surgery patients, who have total costs that are twice as high as surgical costs and 3.5 times as high as persistent medical costs.

Accumulated creatine kinase MB isoenzyme release (sigma CK-MB) during acute myocardial infarction was correlated with biplane left ventricular (LV) angiographic estimates of percent abnormally contracting segment (%ACS) and ejection fraction (EF) in 35 patients who underwent diagnostic angiography at a mean of 33 +/- 4 days post myocardial infarction (MI). Of the 35 patients, 18 had no evidence of prior MI and their sigma CK-MB showed good correlation with %ACS (r = 0.84) and with EF (r = - 0.78). An additional two patients with first (inferior) infarct secondary to stenosis of the right coronary artery proximal to the origin of the right ventricular arterial blood supply had disproportionately large sigma CK-MB, suggesting a combination of LV and RV necrosis. In the 15 patients with prior infarct, there was no significant correlation between sigma CK-MB and %ACS or EF. However, in the subgroup of patients with anterior MI, %ACS correlated with sigma CK-MB, both in patients with no prior MI (r = 0.88, N = 12) and in patients with prior MI (r = 0.69, N = 9). These independent angiographic and enzymatic data suggest that enzymatic infarct size estimates utilizing accumulated CK-MB release may be a valid and reliable clinical measure for assessing the extent of LV necrosis in the setting of acute anterior myocardial infarction. However, limitations may exists in certain cases of inferior MI, probably because of concomitant right and left ventricle necrosis.

Despite the development of trained mobile rescue squads, cardiopulmonary collapse outside the hospital continues to carry a poor prognosis. We examined retrospectively the clinical courses of 19 consecutive coronary unit patients who had experienced prehospital cardiopulmonary resuscitation. Seven patients received basic life support from bystanders within five minutes. Cardiopulmonary resuscitation in the other 12 patients was delayed beyond five minutes pending the arrival of rescue personnel. Six of seven early-resuscitated patients survived compared with six of 12 late-resuscitated patients (P less than 0.01). The early-resuscitated patients were more alert on admission and had lower pulmonary pressures and higher cardiac outputs compared to the late-resuscitated patients. The early-resuscitated patients also had less residual central nervous system and myocardial damage on discharge than the late-resuscitated patients. On follow-up, three early-resuscitated patients had returned to full-time work compared with none in the late group. Training laymen to initiate early basic life support can benefit the cardiopulmonary collapse victim.