An unusual variant of familial preexcitation.
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Biomedical subjects
Publications and source records attributed to D B Hackel.
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To determine the prognostic implications of an early peak in plasma MB creatine kinase (MB CK) in patients with acute myocardial infarction who were not treated with an acute intervention, 342 patients with myocardial infarction confirmed by MB CK were retrospectively studied. The patients were classified into those with an early peak MB CK (less than or equal to 15 hours after the onset of symptoms, n = 84) and those with a late peak MB CK (greater than 15 hours after the onset of symptoms, n = 258). Patients with an early peak MB CK were slightly older, were more frequently female and had a higher incidence of prior myocardial infarction, congestive heart failure and arrhythmias compared with patients with a late peak MB CK. Patients with an early peak MB CK more frequently presented with ST segment depression (23 versus 11%, p less than 0.01), with anterior location of ischemia or infarction (71 versus 52%, p less than 0.01) and with a lower mean left ventricular ejection fraction (41.4 versus 47.4%, p less than 0.01). Despite more extensive left ventricular dysfunction at initial presentation, patients with an early peak MB CK had a smaller mean MB CK infarct size index (12.6 versus 18.9 g-Eq/m2, p less than 0.01), with no difference in the incidence of in-hospital complications, including death. The early left ventricular dysfunction improved in the patients with an early peak MB CK, evidenced by a 4.5% increase in ejection fraction from admission to 10 days after infarction, whereas the ejection fraction did not improve in patients with a late peak MB CK. However, the patients with an early peaking MB CK had myocardium in jeopardy as reflected by a higher incidence of ST segment depression and a decrement in the global left ventricular ejection fraction with exercise. The 4 year life table estimate for the rate of recurrent myocardial infarction after hospital discharge was higher in patients with an early peak MB CK (33 versus 22%, p less than 0.05), with an even more striking difference in the 4 year estimate for the rate of fatal recurrent infarction (20 versus 8%, p less than 0.001). The 4 year mortality estimate was markedly higher in hospital survivors with an early peak MB CK than in those with a late peak (47 versus 19%, p less than 0.0001) and, even after adjustment for differences in baseline characteristics, the residual excess mortality in those with an early peak was still significant (p less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)
The purpose of this study was to determine at necropsy the morphologic consequences of percutaneous transluminal coronary angioplasty performed during acute myocardial infarction. The heart was examined in four patients who died between 6 hours and 4 days after coronary angioplasty. The patients had angioplasty of the left main coronary artery (one patient), left anterior descending coronary artery (two patients) and left circumflex coronary artery (one patient). Necropsy revealed residual stenosis, intimal hemorrhage and plaque disruption in all four patients. Also noted were distal embolization of plaque elements (two patients) and thrombotic occlusion of the coronary artery (one patient). In conclusion, the morphologic changes after angioplasty are varied. These changes illustrate the mechanisms of angioplasty and some of the complications that can be expected in a small number of cases. The morphologic changes associated with coronary angioplasty are similar in patients undergoing elective or emergency angioplasty although medial dissection was not observed in these patients with an evolving myocardial infarction.
To study whether myocardial infarction differs in patients with and without ventricular tachycardia, the hearts of 22 deceased patients with ventricular tachycardia and 21 deceased control patients were analyzed quantitatively. The hearts from the ventricular tachycardia group were heavier and more dilated than those from the control group. Histologic analysis of a representative cross section from each heart showed that the ventricular tachycardia group had larger, more solid infarcts than did the control group. The ventricular tachycardia group also had a greater area of spared subendocardium, more hydropic change of the spared subendocardium, and more "ribbon type" spared subendocardium, which was defined as spared subendocardium of uniform contour 1 mm thick or less. The ventricular tachycardia group was divided into a subacute subgroup (n = 14, dying less than or equal to 10 weeks after infarction) and a chronic subgroup (n = 8, dying greater than 10 weeks after infarction). The infarcts of the subacute ventricular tachycardia group were more solid and had a greater amount of ribbon type spared subendocardium than those of the chronic ventricular tachycardia group. This information can serve as a baseline for the evaluation of animal preparations of tachycardia and, when combined with knowledge of the location of the arrhythmogenic region furnished by intraoperative mapping, should lead to better understanding of the anatomic substrate for ventricular tachycardia.
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.
A case of so-called mesothelioma of the atrioventricular node is presented. Controversy exists as to whether this lesion is of mesodermal or endodermal origin. The light and electron microscopic morphologic characteristics in this case were identical to those reported previously. The glandular component produced mucin that resisted digestion with both hyaluronidase and diastase; this staining pattern is characteristic of endodermal rather than of mesodermal tissue. Immunohistochemical methods demonstrated abundant carcinoembryonic antigen (CEA) in the cytoplasm of the cells composing the lesion. The presence of CEA strongly argues for an endodermal origin, since this antigen characterizes tissue derived from endoderm and is generally absent from mesoderm. The lesion probably represents endodermal foregut tissue that is displaced during embryogenesis. As such, it is not a true neoplasm. It is proposed that this lesion be designated "congenital endodermal heterotopia of the atrioventricular node."
The accuracy of interpretation of coronary cineangiography by two independent observers was tested against postmortem findings in 27 patients who died within 6 months of cardiac catheterization. Variations in cineangiographic interpretations between the angiographers were also evaluated. Two patients had normal coronary arteries, while the remaining 25 patients had significant coronary artery disease. Significant stenosis was defined as 75% or greater reduction in luminal diameter. Of 326 coronary segments that could be evaluated postmortem, 15% could not be evaluated cineangiographically. The respective overall accuracy of the two observers was 89 and 88% with an accuracy of 96 and 100% for the left main coronary artery, 91 and 93% for the left anterior descending artery, 84 and 86% for the right coronary artery and 89 and 79% for the left circumflex coronary artery. Cineangiographic assessment of luminal status distal to a significant proximal lesion was possible in more than 70% of major vessels with accuracy levels of 86% for both observers. Of 96 distal vessels inadequately opacified cineangiographically, 49 (52%) were found to be free of significant lesions. Both angiographers agreed in their assessment of 86% of the 340 coronary segments. Interobserver agreement was significantly better for the left main, right and left anterior descending coronary arteries than for the left circumflex coronary artery (p less than 0.05). Accuracy was 93% for 244 segments that were adequately opacified and assessed the same by both angiographers. Cineangiography can thus be used to evaluate coronary anatomy with a high degree of accuracy and minimal interobserver variability.
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.
A 37-year-old man with an evolving anterior myocardial infarction received intracoronary thrombolytic therapy six hours after its onset. The restored coronary artery patency was recorded angiographically in the left anterior descending coronary artery (LAD). He died 28 hours after administration of the therapy. Uniform and severe interstitial hemorrhage was present in the area of myocardial necrosis. The distribution of hemorrhage and myocardial necrosis corresponded with the vascular bed of the LAD and was thus consistent with experimental studies that concluded that the hemorrhagic areas were probably confined to muscle that was already necrotic.
This study evaluated by quantitative autopsy correlation a previously developed scoring system for estimating the size of myocardial infarcts based on the QRS complex of the electrocardiogram. This system was tested using electrocardiograms from patients with infarcts shown by autopsy to predominate in the inferior third of the left ventricle. The study was limited to patients whose electrocardiogram did not indicate left or right ventricular hypertrophy, left or right bundle branch block, or left anterior or posterior fascicular block. Thirty-one patients from 6 medical centers met these criteria. In the electrocardiogram of 28 of the 31 patients (90%), lead a VF exhibited a Q wave of at least 30 ms. The correlation coefficient between the total QRS score and the percent infarction of the left ventricle was 0.74. In patients without confounding factors in the electrocardiogram and with single infarcts, the electrocardiogram provides a marker for infarcts in the inferior third of the left ventricle and a quantitative QRS scoring system provides an estimate of infarct size.
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The coronary arteries in patients who die of an acute myocardial infarction may be anatomically normal or they may have a combination of lesions. They may show only marked atherosclerosis, with or without special features such as intramural hemorrhage or plaque rupture. There may also be thrombotic occlusion of the lumen of the artery. Whether this thrombotic process usually occurs before the myocardial infarction or whether it sometimes follows and results from the infarct is not known.
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.
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.
Because of the value of cryoablation of the atrioventricular (AV) conduction system in treatment of refractory cardiac rhythm disorders, the anatomic effects of cryoablation on the cardiac conduction system must be defined. In this report we summarize studies done on four patients who had intractable recurrent supraventricular tachyarrhythmias or or refractory atrial flutter-fibrillation. They were treated by cryoablation of the AV conduction system and died 8-360 days postoperatively. Serial sections of the AV conduction system were studied. Cryoablation produced lesions that completely destroyed most of the AV node in three cases, the penetrating portion of the His bundle in all four cases, and the branching portion of the His bundle in two cases. The right bundle branch was not involved markedly in any case. The lesions were discrete and sharply delimited; the patient who died 8 days postoperatively had hemorrhage, necrosis and slight inflammatory infiltrate; patients who survived for 49-360 days showed collagen deposition. The AV nodal artery and its branches showed slight to marked intimal thickening in three cases. Small, partly organized thrombi were present just behind the tricuspid valve in two patients. We conclude that cryoablation of the AV conduction system produced discrete cardiac lesions that did not markedly damage the tricuspid valve or aorta.
Myocardial blood flow and left ventricular oxygen utilization were studied in verapamil-treated and untreated pentobarbital-anesthetized dogs subjected to hemorrhagic shock. Blood loss was similar in both groups. The dogs treated with verapamil (n = 15) during shock had a slower heart rate and lower left ventricular oxygen utilization than the untreated dogs (n = 14). Nevertheless, the treated dogs had a significantly higher myocardial blood flow and were able to maintain a higher cardiac index. Thus, verapamil has beneficial hemodynamic and metabolic effects that preserve myocardial function. These effects may explain the improved survival and protection of the heart against anatomic lesions, which have been demonstrated previously in dogs treated with verapamil during hemorrhagic shock.
A study correlating the electrocardiographic findings and the histology of the atrioventricular (AV) conduction system was carried out in 14 cases with chronic complete AV block and in 13 cases without chronic complete AV block. Patients with chronic complete AV block were divided into two groups, based on the width of the QRS complex. The QRS complexes were narrow (less than 0.12 second) in four cases (group 1) and wide (greater than or equal to 0.12 second) in 10 cases (group 2). In group 1, the main lesion was located in the penetrating portion of His bundle (Hisp) in one heart, in the branching portion of the His bundle (Hisb) in another and in the combined regions of Hisb and the left bundle branch in two. Three of the four cases in group 1 had idiopathic fibrosis of the conduction system and one had calcific nodules in the central fibrous body. In group 2, the main lesion was located in Hisb in two cases, in the combined regions of Hisb and the right bundle branch in one, in the Hisb and in the bilateral bundle branches in two, and in the bilateral bundle branches in five. All cases in group 2 were of the idiopathic type, except case 5, which had calcific aortic stenosis. In 13 cases without chronic complete AV block the AV conduction system was histologically normal, except for slight-to-moderate aging changes in the His bundle or the bundle branches. Lesions of the Hisb, which is believed to be the "distal His" electrophysiologically, may induce complete AV block with narrow or wide QRS complexes, depending upon the severity of the lesions in Hisb or adjacent bundle branches.
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