Postmortem Angiography Research Articles

Pulmonary Metastases. Pathological Anatomy

In 88 operative specimens topography, size and histopathological findings of lung metastases were analyzed. The stages of formation of metastases as the phase of invasion, embolization and implantation were differentiated by postmortem angiographies investigating the neo-vascularization of the metastases by 20 to 60 micron vessels. Analyses of metastases by morphological quantification of tumor regression after cytostatic therapy and immune histochemical examinations of lung metastases in unknown primary cancer have gained clinical importance.

QRS voltage measurements in autopsied men free of cardiopulmonary disease: A basis for evaluating total QRS voltage as an index of left ventricular hypertrophy

Use of total 12-lead QRS electrocardiographic voltage as a criterion for left ventricular (LV) hypertrophy has been of recent interest. Although upper and lower limits of QRS voltage for individual electrocardiographic leads have been reported in clinically healthy men and women, the upper limit of total 12-lead QRS voltage has not been established in adults free of cardiopulmonary disease by clinical and necropsy criteria. Therefore, the total QRS voltage from all 12 electrocardiographic leads was determined in 30 autopsied men known to be free of cardiopulmonary disease by clinical assessment and by a special cardiac examination using postmortem coronary angiography and chamber partition determination of LV weight. Gross heart weight, LV weight and total QRS voltage are reported. Comparisons were made between disease-free patients and previously reported patients with aortic valve stenosis, aortic regurgitation and cardiac amyloidosis with respect to total QRS voltage and gross heart weight. Total QRS voltage and gross heart weight were significantly greater in patients with severe aortic stenosis (mean 245 mm) and severe aortic regurgitation (mean 274 mm) than in our patients (mean 127 mm). Total QRS voltage was significantly less, whereas gross heart weight was significantly greater in patients with cardiac amyloidosis (mean 101 mm) than in our normal subjects (mean 127 mm). These data provide a basis for evaluating the total 12-lead QRS voltage as a criterion for LV hypertrophy.

Transmural distribution of myocardial infarction: difference between the right and left ventricles in a canine model.

The evolution of myocardial infarction 24 hours after ligating both the right coronary artery and the obtuse marginal branch of the left circumflex coronary artery was examined in 33 anesthetized dogs. Postmortem coronary angiography and a tracer microsphere technique were used to determine risk areas and their collateral blood flows, respectively. The mean weight of the risk areas was 11.3 +/- 0.5 g (mean +/- SEM) in the right ventricle and 10.5 +/- 0.9 g in the left ventricle (NS). The weight of infarcted tissue was 5.7 +/- 0.7 g in the right ventricle and 5.2 +/- 0.9 g in the left ventricle (NS). In both ventricles, infarct weight was linearly related to risk area size, and the percent of risk area necrosis was inversely correlated with the extent of collateral flow at 24 hours of coronary ligation, defined as the mean myocardial blood flow inside the central risk area. Ratios of infarct to risk area between the subendocardial and subepicardial layers were 0.76 +/- 0.06 and 0.28 +/- 0.05 in the right and left ventricles, respectively (p less than 0.01, between ventricles, n = 31), which coincided well with subendocardial-to-subepicardial-flow ratios at 24 hours, ie, 0.86 +/- 0.04 in the right ventricle and 0.32 +/- 0.06 in the left ventricle (p less than 0.01). The regional distribution of myocardial infarction correlated well with flow distribution inside the risk area; the slope of these relations was similar between the subendocardium and subepicardium in the right ventricle, whereas in the left ventricle it was larger in the subendocardium than in the subepicardium. Thus, in the dog, the inherent change in the regional distribution of coronary collateral blood flow is an important modifier in the evolution of myocardial infarction, especially in the left ventricle.

Comparison of macroscopic, postmortem, angiographic and two-dimensional echocardiographic findings of coronary aneurysms in children with Kawasaki disease

To assess why the results of 2-dimensional echocardiography (2-D echo) for diagnosis of coronary aneurysm in patients with Kawasaki disease differed from those of cineangiography, the macroscopic, postmortem, angiographic and 2-D echocardiographic findings of 8 autopsied hearts of infants and children with Kawasaki disease were compared. Postmortem angiography and 2-D echo yielded similar results in aneurysms in which there was no thrombus, organization or marked thickening of the arterial wall. However, in aneurysms with complete or incomplete occlusion of the dilated cavity due to thrombi, organization or marked thickening of arterial wall, angiographic results reflected only the free cavity of the coronary aneurysm, but could not detect the original aneurysm. Two-dimensional echocardiography disclosed an echo-free space representing the original aneurysm, in which some materials, suggesting thrombi or organization, were found. However, it did not reveal whether the aneurysm was occlusive. This finding indicates that the discrepancies between the results of cineangiography and 2-D echo are attributable to the formation of large thrombi, organization or marked thickening of the arterial wall in the aneurysmal cavity. It is clinically important to know these limitations of angiography and 2-D echo.

A comparison of ST segment deviation and calculated solid angle during acute regional ischemia in the isolated canine heart at precordial, epicardial and intramyocardial lead surfaces

Although solid angle analysis has been considered to be reasonable for explaining the distribution of ST segment deviation following ischemia, it has not been tested fully, especially for ST segment changes in various sites at different lead surfaces. Thus, we investigated the applicability of solid angle theory to the mechanism of ischemic ST segment deviation at intramyocardial, epicardial and precordial leads. We used seven isolated, coronary perfused, isovolumic contracting canine hearts in a homogeneous cylindrical volume conductor. ST segment potentials from 246 electrodes were continuously measured during left circumflex coronary artery occlusion for five minutes. The ischemic boundary was obtained from a postmortem angiography, and the solid angle subtended by the ischemic boundary was calculated at every electrode site. Despite the difference between epicardial and precordial ST segment potential distributions, there was a high correlation between measured ST segment potential and calculated solid angle at epicardial (r = 0.86 +/- 0.05, 0.77-0.93), precordial (r = 0.93 +/- 0.05, 0.84-0.99), and intramyocardial leads (r = 0.95 +/- 0.03, 0.91-0.99). We conclude that solid angle analysis can be used to approximate the distribution of ischemic ST segment deviation at different lead surfaces in acute ischemia.

Pathogenetic mechanism of stenosis in the intramural coronary artery.

In order to clarify the pathogenetic mechanism of stenosis in the intramural coronary branch, morphological changes were examined by postmortem coronary angiography and determination of the Coronary Stenosis Index of the Myocardium (CSIM) were made in hearts obtained by autopsy from 10 patients with hypertension, 15 with normotensive myocardial infarction, 25 with hypertensive myocardial infarction, 6 with mitral valvular disease, 7 with aortic stenosis and 14 control subjects. CSIM was significantly higher in patients with hypertension, infarction with hypertension and aortic stenosis than in other three groups, indicating higher incidence of stenosis in those with a left ventricular pressure load. There was no specific correlation between the degree of stenosis of the epicardial coronary artery and that of the intramural coronary branches supplied by the former in any groups examined. Major pathological changes of the intramural coronary branches were muscular hypertrophy of media and proliferation of internal elastic lamella, both observed with a high incidence in vessels with high CSIM values. These findings suggest that intramural pressure which exerted extravascular pressure played an important role in the pathogenetic mechanisms of stenotic changes in the intramural coronary branches.

Myocardial Haemorrhage after Intracoronary Thrombolysis

Clinical, angiographic, and necropsy data of 16 patients who died 1–18 days after streptokinase treatment for acute coronary occlusion are presented. In 8 cases prompt recanalisation was documented clinically by angiography. At post-mortem angiography, thrombolysis was documented in one patient. In the remaining 7 patients the occluded vessel had not been recanalised. All 16 patients had a transmural acute myocardial infarction. In 7 patients with unsuccessful thrombolytic therapy the infarct was anaemic. In the 9 successfully recanalised patients, 3 cases of anaemic infarction and 6 cases of haemorrhagic infarction were observed. Two of the latter also had minor anaemic infarctions. The mean period of time preceding successful recanalisation was significantly shorter in patients having anaemic infarcts (1·9 h) than in those having haemorrhagic infarcts {3·2 h) (P<0·01). Haemorrhagic infarcts were twice as large as anaemic infarcts. The speed of healing of the infarcts appeared to be delayed in haemorrhagic infarcts, as demonstrated in 2 patients. Recanalisation after more than 3 h of coronary artery occlusion is likely to be followed by myocardial haemorrhage in large transmural infarcts.

Post-mortem investigation and quantification of coronary artery disease.

The controversies that exist amongst pathologists about ischaemic heart disease result in part from the widespread use of non-quantifiable techniques in examining the coronary artery tree. Such techniques are used because it is believed that there is no alternative method which does not involve an inordinate expenditure of time, money and effort. This paper describes procedures involving post-mortem coronary angiography which may be used alone or in combination with histological examination to give an immediate, accurate and permanent record of coronary artery disease or allow a far more detailed quantitative investigation of coronary vasculature.

Injuries associated with percutaneous placement of transthoracic pacemakers

Injuries associated with the percutaneous placement of transthoracic pacemakers are poorly documented. We prospectively sought to determine any injuries associated with various placement routes. Six different approaches were used in each of 20 adult patients examined at autopsy. Three parasternal approaches utilized the fifth intercostal space (5ICS). One pacing wire was inserted immediately to the left of the sternum along the parasternal line (5ICS-PS), one pacing wire was inserted 4 cm to the left of the midsternal line (5ICS-4), and the third wire was inserted 6 cm from the midsternal line (5ICS-6). All parasternal needle insertions were directed medially, dorsally, and cephalad toward the right second costochondral junction at an angle of 30 degrees to the skin. Three subxiphoid approaches were inserted through the left xyphocostal notch at an angle of 30 degrees to the skin. One pacing wire was directed toward the right shoulder, one toward the sternal notch, and one toward the left shoulder (SXLS). Injuries were assessed by autopsy, postmortem coronary angiography, and stereoscopic radiography. The 5ICS-PS approach resulted in fewer injuries when compared to all other approaches. Because previous work has demonstrated that the 5ICS-PS, 5ICS-6, and SXLS approaches are more accurate than the other approaches for transthoracic pacemaker insertion, the 5ICS-PS represents an approach that combines reasonable accuracy with the least likelihood for injury in the placement of percutaneous transthoracic pacing wires.

Coronary artery atherosclerosis observed in men over 14 consecutive years.

The incidence of cardiovascular death and myocardial infarction associated with ischemic heart disease has declined over the past 15 years. Whether this is associated with a decrease in the severity of coronary atherosclerosis is unknown. The extent of coronary atherosclerosis in men was determined by postmortem coronary angiography in 505 patients over an observation period of 14 years. Patients were divided into those with ischemic heart disease (42%) and those without (58%). Mean coronary scores showed no significant trends over the 14-year period in those without ischemic heart disease and for the last 10 years in those with ischemic heart disease. In those few patients evaluated early in the study with ischemic heart disease, a significantly lower coronary score was found compared to subsequent years. This study was performed during an era of declining cardiovascular death rates and a declining incidence of myocardial infarction, and suggests that this decline may relate to favorable changes in pathogenesis rather than to a decrease in extent of coronary atherosclerosis.

Diameter of coronary arteries in 36 species of mammalian from mouse to giraffe.

Systematic quantitative investigations were performed in the coronary arteries of 102 hearts of 36 mammal species with an overall more than tenthousandfold difference of their heart weight. After postmortem coronary angiography with a filling pressure of 100 mm Hg x-rays were taken, and the widest diameters of the coronary artery stems were determined. We found a nearly linear correlation between diameter of a standardized coronary artery and virtual diameter of heart, but the increase in diameter of coronary arteries exceeded somewhat that of the diameter of heart especially for heart weights surmounting 100 g. Perhaps relative enlargement of coronary arteries in the bigger hearts contributes to the prevention of large increase of blood flow velocity.

Descriptive characteristics of the electrocardiogram from autopsied men free of cardiopulmonary disease—A basis for evaluating criteria for ventricular hypertrophy

Most measurements establishing standard values for the normal electrocardiogram have been derived from a healthy population, whereas many electrocardiographic interpretations are necessary in hospitalized or seriously ill patients. Therefore, the characteristics of the electrocardiogram were described from 48 autopsied men known to be free of cardiopulmonary disease by clinical assessment and by a special cardiac examination using postmortem coronary angiography and a chamber partition technique. Highest values, mean and standard deviation, and the upper 97.5 percentile or lower 2.5 percentile when appropriate were noted for QRS voltage, QRS axis and duration, and intrinsicoid deflection in V 5 or V 6. Any ST-segment and T-wave changes were noted as well as left and right atrial abnormalities. Twenty-eight electrocardiographic criteria recommended to detect left ventricular hypertrophy and 10 recommended to detect right ventricular hypertrophy were evaluated for percentage of false-positive results and the 97.5 percentile value for each criterion was developed from the present data base. The data in this study can be used as a standard for comparing electrocardiographic variation in middle-aged men with specific relevance for electrocardiographic criteria of ventricular hypertrophy.

Delayed thrombolysis of streptokinase-resistant occlusive thrombus: Documentation by pre- and postmortem coronary angiography

Delayed thrombolysis of streptokinase-resistant occlusive thrombus: Documentation by pre- and postmortem coronary angiography

Significance of the angiographic morphology of localized coronary stenoses: histopathologic correlations.

Postmortem coronary angiographic morphology was correlated with histologic sections of 73 localized subtotal coronary artery stenoses (50-99% reduction of luminal diameter) to determine whether complicated or uncomplicated atherosclerotic lesions could be detected angiographically. Lesions were divided into two types, according to angiographic morphology: Type I stenoses had smooth borders, an hourglass configurations, and no intraluminal lucencies; type II stenoses had irregular borders or intraluminal lucencies. Histologic sections were also divided into two types: "uncomplicated" stenoses had fatty or fibrous plaques with intact intimal surfaces and no superimposed thrombus; "complicated" stenoses manifested plaque rupture, plaque hemorrhage, superimposed partially occluding thrombus, or recanalized thrombus. Among 35 lesions with type I angiographic morphology, four (11.4%) were complicated lesions histologically. Among the 38 stenoses showing type II angiographic morphology, 30 (78.9%) were complicated lesions. Postmortem angiography thus had a sensitivity of 88% and specificity of 79% for detecting complicated stenoses on the basis of irregular borders or intraluminal lucencies. Pathologic studies have shown that acute occlusive thrombosis of a coronary artery is usually associated with complicated atherosclerotic stenoses. Thus, complicated lesions represent a greater risk factor for acute myocardial infarction or sudden death than do uncomplicated lesions. This study suggests that coronary stenoses characterized angiographically by irregular borders or intraluminal lucencies are probably the clinically more dangerous "complicated" type.

Balloon catheter dilatation of stenotic renal artery anastomoses. Experiments in the pig.

Stenotic renal artery anastomoses were produced in pigs in order to investigate the effects of transluminal angioplasty. Six weeks after surgery unilateral dilatation with a modern balloon catheter was performed in 8 pigs. These animals were reexamined with angiography and pressure gradient recording 8 to 10 weeks after dilatation and with post-mortem angiography 8 to 10 weeks later. Only 2 arteries had minimal residual stenoses, while in 6 arteries the stenoses were completely eliminated. Microscopic examination showed thinning of the fibrotic vessel wall, with defects in the internal elastic lamina.

Effects of chronic hypertension and left ventricular hypertrophy on the incidence of sudden cardiac death after coronary artery occlusion in conscious dogs.

When acute myocardial infarction occurs in patients with hypertension and left ventricular hypertrophy (LVH), the incidence of sudden cardiac death increases markedly. Possible explanations include increased size of the occluded vascular bed secondary to more extensive atherosclerotic coronary vascular disease in the presence of hypertension, decreased coronary reserve secondary to LVH, and intrinsic electrophysiologic abnormalities in hypertrophied cardiac muscle. To explore these possibilities, we produced acute circumflex coronary occlusion during the resting, conscious state in 32 control dogs and in 28 dogs with hypertensive LVH. Before coronary occlusion, mean arterial pressure was 96 +/- 0.1 mm Hg in control dogs and 125 +/- 5 mm Hg in dogs with hypertensive LVH (p less than 0.01). The control left ventricular/body weight ratio was 4.5 +/- 0.1 g/kg, compared with 6.1 +/- 0.1 g/kg in hypertensive LVH (p less than 0.01). Cumulative mortality at 6, 24 and 48 hours was 9%, 13% and 16% in control dogs and 32%, 43% and 54%, respectively, in dogs with hypertensive LVH (all p less than 0.01 vs control). The perfusion fields of the occluded vessel defined by postmortem coronary angiography were similar in the two groups (31 +/- 2% of left ventricular mass for control vs 29 +/- 2% for hypertensive LVH). Thus, the increased incidence of sudden cardiac death after coronary artery occlusion in hypertensive LVH dogs cannot be explained by increased size of the occluded vascular bed and is probably related to the decreased coronary reserve or intrinsic electrophysiologic abnormalities that characterize pressure-induced hypertrophied cardiac muscle.

Transcatheter fiberoptic laser coagulation of blood vessels.

In ten rabbit ears the central auricular artery was percutaneously catheterized and subjected to doses of laser energy transmitted through a flexible optical fiber within the artery. Arterial occlusion was not produced in the initial three ears using energy levels less than 600 mW. Higher levels of laser energy, in the range of 800-1000 mW, caused arterial coagulation in six of the remaining seven rabbit ears. Serial observations by transillumination of the ears, postmortem angiography, and histologic examination demonstrated complete arterial ablation. The experiments showed that segmental arterial ablation is feasible using an intra-arterial optical fiber to direct laser energy to a specific arterial target. Technical refinements and potential therapeutic application are discussed.

Salvage of ischemic myocardium by dipyridamole in the conscious dog.

We investigated the effect of i.v. dipyridamole, a potent small-vessel coronary vasodilator, on myocardial infarct size in conscious dogs. Dipyridamole, 7-9.7 microgram/kg; 15 dogs) or saline (15 dogs) was infused for 6 hours beginning 10 minutes after acute permanent occlusion of the mid-circumflex coronary artery. After sacrifice, 48 hours after occlusion, stereoscopic postmortem angiography was used to define the mass of the occluded coronary bed. Infarct size was determined by planimetry of weighed, unstained left ventricular slices. Dipyridamole produced a striking reduction in mean infarct mass compared with control (3.1 g vs 13.2 g, p less than 0.001), while mean occluded bed mass was similar (30.3 g vs 32.7 g, NS). As a percentage of the occluded bed, mean infarct size was reduced from 36.8% to 8.6% ( p less than 0.001). Mean arterial blood pressure declined approximately 10% after dipyridamole. Heart rate and left atrial pressure did not change significantly. Collateral blood flow, measured with 8- mu radioactive microspheres, increased in all regions during dipyridamole infusion. The infarct center and border regions had sustained increases over 6 hours of 23-80%, while nonischemic regions demonstrated a diminishing response over time, with a large (98-125%) increase 10 minutes after infusion and a smaller (22-25%) increase 6 hours later. Although antiplatelet or local metabolic effects cannot be excluded, the myocardial salvage produced by dipyridamole was most likely due to the increase in collateral blood flow.

Nodular regenerative hyperplasia of the liver associated with macroglobulinemia: A clue to the pathogenesis

Nodular regenerative hyperplasia of the liver is an infrequent condition characterized by transformation of the hepatic parenchyma into nodules with only mild fibrosis. Little is known about the etiology except that there is usually an underlying chronic disease, such as Felly's syndrome, which antedates the development of clinical liver disease. It is poorly understood how the associated diseases contribute to the pathogenesis of nodular regenerative hyperplasia. Presented are four cases of nodular regenerative hyperplasia in which macroglobulinemia was also present. This new association suggests to us a hypothesis for the pathogenesis of nodular regenerative hyperplasia. Histologic examination of the livers in these and other cases of nodular regenerative hyperplasia reveals widespread obliteration of the small portal veins. Postmortem angiography of one liver in the present series demonstrated that the nodules were well perfused and that the atrophic areas were poorly perfused with portal blood. This supports the view that atrophy of lobules results from a lack of portal blood supply and that nodules develop from lobules well supplied with portal blood. In each of the clinical conditions associated with nodular regenerative hyperplasia, including macroglobulinemia, inflammatory or thrombotic vascular lesions are found in many organs. Therefore, nodular regenerative hyperplasia may be the hepatic expression of a more widespread vascular disease.

Postmortem coronary angiography and histological investigation of the conduction system of the heart in sudden unexpected death due to coronary heart disease.

This study has been performed applying postmortem coronary angiography and histological investigation of the conduction system of the heart in 21 persons who died suddenly and unexpectedly because of coronary sclerosis. This "coronary group" is compared with a sex and age matched control group of 24 persons. Acute vascular lesions were found in 20 persons (95.2%), fresh infarctions in 10 (45%), heart rupture in 2 (9.5%) and old infarctions (indicated by localized fibrosis) in 7 (33.3%). The coronary arteries were graded using WHO's recommendations from 1958. Arteriosclerosis of the major coronary arteries was significantly more extensive in the "coronary group". The origin and course of the arteries to the conduction system were located by postmortem coronary angiography. The right coronary artery supplied these arteries in the majority of cases (sinus node artery 77%, a.-v. node artery 85%). A significantly greater degree of arteriosclerosis could be demonstrated histologically in the sinus node artery in the "coronary group". In both groups the degree of arteriosclerosis was greater in the a.-v. node artery than in the sinus node artery. The conduction system was investigated using Hudson's method. There were only 3 cases of infarction in the conduction system, possibly due to its greater resistance to damage from anoxia. In all patients "non-specific changes" (hemorrhage, small cellular infiltrations and/or degeneration) were found and these changes can, therefore, be of no pathophysiological importance in this group of patients. The degree of fibrosis and the amount of fat was semiquantified. Six patients in the "coronary group" had moderate fibrosis around the left sided fibres of the bundle of His. This leads to the conclusion that these changes might play a role in the fatal course, and that some cases of sudden, unexpected cardiac death can be explained by pre-existing fibrosis in the conduction system.