Donald B. Hackel

Evaluation of a QRS scoring system for estimating myocardial infarct size

This study correlated the location and size of posterolateral myocardial infarcts (MIs) measured anatomically with that estimated by quantitative criteria derived from the standard 12-lead ECG. Twenty patients were studied who had autopsy-proved, single, posterolateral MIs and no confounding factors of ventricular hypertrophy or bundle branch block in their ECG. Left ventricular anatomic MI size ranged from 1 to 46%. No patient had a greater than or equal to 0.04-second Q wave in any electrocardiographic lead and only 55% had a 0.03-second Q wave. A 29-point, simplified QRS scoring system consisting of 37 weighted criteria was applied to the ECG. Points were scored by the ECG in 85% of the patients (range 1 to 8 points). MI was indicated by a wide variety of QRS criteria; 19 of the 37 criteria from 8 different electrocardiographic leads were met. The correlation coefficient between MI size measured anatomically and that estimated by the QRS score was 0.72. Each point represented approximately 4% MI of the left ventricular wall.

Evaluation of a QRS scoring system for estimating myocardial infarct size. II. Correlation with quantitative anatomic findings for anterior infarcts

The ability of an independently developed QRS point score to estimate the size of infarcts predominantly within the anterior third of the left ventricular was evaluated by quantitative pathologic-electrocardiographic correlation. The study was limited to 21 patients with a single infarct documented by postmortem examination, for whom an appropriately timed standard 12 lead electrocardiogram was available that did not exhibit signs of left or right ventricular hypertrophy, left or right bundle branch block or anterior or posterior fascicular block. At necropsy the heart was cut into five to seven slices. The location and size of the infarct was quantitated by computer-assisted planimetry of the slices. The electrocardiogram of 19 (90 percent) of the patients exhibited either a Q wave or an R wave of no more than 20 ms in lead V2. The infarct in the two patients without this electrocardiographic finding was small, occupying 2 and 3 percent of the left ventricle, respectively. The percent infarction of the left ventricle correlated with the QRS point score (r=0.80). Thus in patients without complicating factors in the electrocardiogram and with a single infarct, the electrocardiogram provides a marker for infarction in the anterior third of the left ventricle and permits estimation of infarct size.

Comparison of angiographic and postmortem findings in patients with coronary artery disease

The accuracy of coronary cineangiography in predicting the degree of stenosis in coronary arteries was evaluated by comparing autopsy and premortem cineangiographic findings in 25 patients. Coronary cineangiograms and autopsy specimens were reviewed independently by two cardiologists and two pathologists. Identical diagrams dividing the cononary arteries into 12 segments were used by both groups to record the location and degree of stenosis observed. Cineangiographic findings were in agreement with pathologic findings (less than 25 percent difference in cross-sectional luminal area) in 178 (79 percent) of the 226 segments examined, but overestimated the degree of stenosis in 13 (6 percent) and underestimated it in 34 (15 percent). Thus, cineangiography appears to be a reliable tool in evaluating coronary artery disease. When diagnostic errors are made, they are usually underestimations of the degree of disease; common causes of error are circumferential stenosis, eccentric lesions, obstruction of view by artifical valves and poor opacification due to severe proximal stenosis.

The anatomy and blood supply of the papillary muscles of the left ventricle

Abstract The supply of blood to the papillary muscles is segmental in distribution, and reaches the muscle from large penetrating branches originating from epicardial vessels located radially outward from the muscle. The tip, mid-portion, and base generally receive their vascular supply from separate tributaries which have a radial arrangement. Fibrosis of the papillary muscles is most often associated with occlusive disease of the large coronary vessels. The vascular alteration accompanying this fibrosis is of two types: (1) a fine overgrowth of Class A vessels, without interruption of the Class B vessels, and (2) an interruption of all channels, with enlargement of subendocardial vessels, suggesting the utilization of these vessels in the formation of collaterals past the occluded area.

The vascular supply of the left ventricular wall: Anatomic observations, plus a hypothesis regarding acute events in coronary artery disease☆

Abstract Postmortem injection studies of the left ventricular wall in 58 human hearts have revealed a characteristic distribution of vessels: those which divide quickly (Class A), and those which penetrate to the subendocardial layers, forming multiple anastomosing arcades (Class B). This subendocardial plexus appears to play an important role as a collateral channel in coronary disease. These anatomic features suggest an explanation for certain features observed in patients with coronary artery disease. This concept assigns a permissive role to the large occlusive lesions of the coronary arteries. Such lesions make the potentially ischemic focus distal to the occlusion dependent on collateral flow through the subendocardial plexus, thus permitting dynamic factors that modify this collateral circulation to become critically significant.

Combined right and left ventricular infarction: Pathogenesis and clinicopathologic correlations☆

Abstract An autopsy examination was made in 102 consecutive cases of fatal myocardial infarction that occurred in a coronary care unit. Thirty-five of the patients (34 percent) were found to have right ventricular infarction. All of the right ventricular infarcts were associated with transmural infarction of the posterior left ventricle or the interventricular septum, or both. The group with right ventricular infarction was compared with that without right ventricular infarction. Both groups had a predominant pattern of coronary arterial atherosclerosis consisting of severe stenosis of the proximal left anterior descending and proximal right coronary arteries with variable involvement of the left circumflex and left main coronary arteries. There was no significant difference between the two groups in severity or distribution of coronary arterial atherosclerosis. However, the group with right ventricular infarction had twice as many recent coronary arterial occlusions as did the group with left ventricular infarction and at least one recent coronary arterial lesion was present in 86 percent of those with right ventricular infarction, compared with only 30 percent of the group with left ventricular infarction. The majority of the acute coronary arterial lesions in both groups were thrombotic, but many intramural hemorrhages within atherosclerotic plaques were also found. In both groups the greatest number of recent coronary arterial occlusions was in the proximal right coronary artery, but the acute lesions were distributed throughout the coronary arterial tree.

Comparison of enzymatic and anatomic estimates of myocardial infarct size in man.

Enzymatic estimates of myocardial infarct size based on plasma levels of MB creatine kinase (MB-CK) were compared with anatomic infarct size in 49 human hearts obtained at autopsy. The patients studied had been enrolled in the Multicenter Investigation of Limitation of Infarct Size (MILIS) study program within 18 hr of the onset of acute infarction and were treated at one of five participating hospitals. Infarct size was estimated from serial measurements of plasma MB-CK made at the core laboratory for CK analysis. Hearts obtained at autopsy were studied independently by the core pathology laboratory without knowledge of the MB-CK levels or clinical results. Data from the two laboratories were compared at the data coordinating center. Of 49 hearts, 12 were excluded either because anatomic infarct size could not be established or because the infarct occurring at the time of enrollment in the MILIS study could not be distinguished with certainty from other infarcts. Of the remaining 37 hearts, peak MB-CK level was available in 36, but samples sufficient for estimation of infarct size were available in only 25. The overall correlation coefficient (Spearman) was .87 for these 25 hearts, indicating that enzymatic estimates of infarct size correlate closely with anatomic measurements. The results indicate that CK estimates of myocardial infarct size represent a valid clinical end point for assessing myocardial infarct size, and the effect of therapy thereon, in groups of treated and control patients.

DIABETES MELLITUS IN THE SAND RAT INDUCED BY STANDARD LABORATORY DIETS.

During an attempt to establish a laboratory colony of the sand rat (Psammomys obesus) we found that this animal invariably became obese and developed severe diabetes mellitus when fed on commercial laboratory rat feed, but remained normal when fed on fresh vegetables only. The signs of diabetes included elevated blood glucose, excessive glucose and ketone bodies in the urine, and cataracts. The diabetic animals showed degeneration of the pancreatic insulin producing tissue (beta-cells).

Antiplatelet Therapy Reduces Aortic Intimai Hyperplasia Distal to Small Diameter Vascular Prostheses (ptfe) in Nonhuman Primates

While the use of prosthetic grafts in small diameter arterial reconstruction is required when suitable autogenous graft material is unavailable, late occlusion of prosthetic grafts caused by proliferative lesions has been described. This study evaluated the suitability of 3-mm (ID) microporous polytetrafluoroethylene (PTFE) Gore-Tex grafts inserted in the abdominal aorta of eight nonhuman primates (Macaca fascicularis), and the effects of prolonged antiplatelet treatment on both graft patency and the development of intimal hyperplasia in the adjacent vasculature. Four monkeys received antiplatelet medication consisting of aspirin (163 mg twice daily) and dipyridamole (25 mg twice daily). When killed at four months following graft insertion, all four grafts in the antiplatelet medicated group were patent, while in the control group, only two of four grafts were patent. Histologic examination and quantitative photogravitometric evaluation of the degree of luminal narrowing were performed on all grafts and the adjacent vasculature. These studies revealed that while all graft and aortic segments showed varying amounts of intimal thickening, occlusions in the control animals were related to intimal hyperplasia in the host aorta at the site of the distal anastomosis. Intimal hyperplasia in all aortic segments examined distal to the graft was significantly reduced by antiplatelet therapy. Electronmicroscopy showed that smooth muscle cells were the predominant cells of the intimal thickening of the aorta (intimal hyperplasia), and that proliferation of these cells did not extend into the graft itself. The predominant cell population of the intimal thickening of the graft were of the myofibroblast type (neointimal hyperplasis). The luminal surface of the graft was lined with cells that had some but not all of the characteristics of mature endothelial cells. In vitro studies confirmed global interference with platelet function and arachidonic acid metabolism in medicated animals. Medication inhibited platelet cyclo-oxygenase without affecting platelet lipoxygenase, thromboxane synthetase, or prostacyclin-like activity in undisturbed arteries. This study shows that severe intimal hyperplasia develops rapidly in the recipient vessel adjacent to small diameter Gore-Tex grafts, and that the severity of the response is reduced by antiplatelet agents. Histologic examination revealed that the intimal thickening in the graft and the adjacent aortic segments were composed of cells that were not morphologically identical, suggesting two separate aetiologies and the possible need to use different approaches in their prevention.

Quantitative analysis of right and left ventricular infarction in the presence of postinfarction ventricular septal defect

To quantitate the amount of right and left ventricular infarction in patients dying with postinfarction ventricular septal defect (PIVSD), hearts from 54 patients with anterior or inferior myocardial infarction were studied at autopsy. Fifteen hearts had myocardial infarction with PIVSD and 39 hearts had infarction without PIVSD and were used as a comparison group. All infarcts were sized histologically and the percent of each ventricle infarcted was quantitated by computer-assisted planimetry. The pathologic substrate for PIVSD was diffuse coronary artery disease with acute thrombosis resulting in transmural confluent infarction. Within the PIVSD group, there was significantly more left ventricle involved in anterior infarctions than in inferior infarctions (p less than .04). Conversely, there was more right ventricular infarction in inferiorly located myocardial infarctions with resulting PIVSD (p = .059). When infarctions resulting in PIVSD were compared with infarctions not resulting in PIVSD, the PIVSD group was characterized by larger left and right ventricular infarcts irrespective of infarct location (p less than .003). The incidence of right ventricular infarction was 100% in the PIVSD group (p less than .0001). Twelve of the 15 patients with PIVSD (80%) developed cardiogenic shock within 48 hr of septal rupture. The high incidence of shock and the rapid deterioration may have been secondary to right ventricular infarction in these patients. Therefore, infarcts resulting in PIVSD and subsequent death are characterized by a high incidence of right ventricular infarction. Significantly more infarction of the right ventricle is seen in either anterior or inferior infarctions resulting in PIVSD compared with infarctions not resulting in PIVSD. PIVSD complicating inferior infarctions is associated with the greatest amount of right ventricular infarction.