Amyloid disease of the heart.

A 70-year-old woman with a history of hypertension had been well until 3 years before when she developed atrial fibrillation and subsequently congestive heart failure. The heart failure became worse and she had three fainting spells. Low voltage on electrocardiogram and global hypokinesis on echocardiography were suggestive of cardiac amyloidosis. The patient died suddenly of intractable ventricular fibrillation. Autopsy confirmed heavy infiltration of the myocardium by amyloid.

Idiopathic dilated cardiomyopathy.

A 43-year-old man had a 9-year history of congestive heart failure manifested by an enlarged heart and symptoms of shortness of breath and chest discomfort. Heart failure had been preceded by a "viral illness" and he had been a heavy alcohol user until that time. Autopsy showed congestion and edema characteristic of heart failure and cardiomegaly with biventricular dilatation. Either viral or alcoholic disease, or both, could have been the cause of the cardiac problems.

Cor pulmonale caused by recurrent pulmonary emboli.

A 53-year-old black man developed femoral thrombophlebitis in 1983 following a Harrington nail implantation in his first lumbar vertebral region. There was evidence of pulmonary embolization at that time and recurrently until he developed ventricular fibrillation and died in 1987. The terminal event followed a hypotensive episode during the course of a right ventricular catheterization. Autopsy confirmed the clinical impression that he had multiple recurrent thromboemboli to his lungs. After several years of embolization, the pulmonary arterial circulation was sufficiently occluded to result in pulmonary hypertension. Cor pulmonale was produced, with congestive heart failure leading to a progressively downhill course in the 4 months before his death.

Congestive heart failure in a patient with systemic hypertension.

A 70-year-old man developed hypertension many years previously and had a bout with severe congestive heart failure 4 to 5 years before his death. Autopsy showed congestion and edema characteristic of heart failure, and enlarged heart, and slight focal interstitial left ventricular fibrosis, but only slight to moderate coronary atherosclerosis.

Acute myocardial infarction with ventricular septal rupture.

The interventricular septum is one of the three main sites at which the myocardium can rupture. The features of the interventricular septal rupture that occurred in a 72-year-old woman are characteristic of interventricular septal ruptures in general: (1) they occur most commonly in elderly women; (2) the most common site is the mid-portion of an acute, transmural anteroseptal apical infarct; (3) they are also most common during the patient's first heart attack; (4) the clinical diagnosis of acute myocardial infarct is confirmed by both ECG and by serum enzyme levels; (5) the usual time of the rupture is 3-10 days after the onset of the infarction (it occurred after 3 days in our patient); (6) a new cardiac murmur usually is heard and the patient frequently goes into shock; (7) the diagnosis can be confirmed by a step-up in pO2 levels from right atrium to right ventricle; (8) the usual cause is severe old coronary atherosclerosis with a recent thrombotic occlusion as the final precipitating event.

Acute myocardial infarction with papillary muscle rupture.

The subject of this report is a 57-year-old obese, hypertensive woman who had been well until the onset of severe chest pain and hypotension. She had to be defibrillated four times on her way to the hospital. The diagnosis of acute inferior-posterior infarction was made by electrocardiogram (ECG) and there was a markedly elevated serum creatine kinase (CK) (including the MB fraction). The patient had a very low cardiac output and ejection fraction. A lung scan revealed possible pulmonary embolism for which she was anticoagulated. She remained hypotensive and hypoxemic and, on Day 17 of her hospital stay, she had a bout of severe dyspnea. A new systolic murmur was heard and the clinical diagnosis of ruptured papillary muscle was made and confirmed by echocardiography, and later at autopsy. All three coronary arteries were severely atherosclerotic and, in addition, the right coronary artery was completely closed by a thrombus. This case clearly illustrates the major pathological changes in the heart that correlate with the clinical findings in patients with a myocardial infarct that is complicated by left ventricular papillary muscle rupture. The pathophysiological effects of this condition, as illustrated in this case report, include the following:1. The posterior papillary muscle wa s almost completely separated from its base, with only a thin strip of muscle intact. The mistral valve thus was insufficient (a "flail valve''); this markedly reduced the ejection fraction of the left ventricle, increased its end-diastolic volume and pressure, produced a damming of blood in the pulmonary circulation, and this resulted in the pulmonary edema seen on the chest x-ray.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute circumferential subendocardial infarction.

A 48-year-old black man had his first attack of chest pain on exertion, radiating to both arms, in December 1982 (angina pectoris). It was undoubtedly preceded by a period of asymptomatic coronary atherosclerosis of unknown duration. The first anginal attack was followed by three to four similar episodes over the next four months. The attacks became more prolonged, frequent, and severe thereafter (so-called "pre-infarct" angina), and six days later the patient showed signs of having developed actual myocardial necrosis. The patient underwent saphenous vein coronary artery bypass surgery but could not be weaned from the pump. He died late on the day of surgery. He was found at autopsy to have severe old three-vessel coronary artery disease with the myocardial changes that would be expected from the severe global ischemia to which this heart was undoubtedly subjected. Several basic and important differences between this sort of a circumferential subendocardial infarct and a transmural infarct are discussed, as is the basis for the striking subendocardial hemorrhage.

Very early acute myocardial infarct treated with streptokinase and balloon angioplasty.

A 57-year-old man developed anginalike chest pain for the first time but there was no objective evidence of an infarct (i.e., EKG and serum enzymes were normal). After 12 days the pain increased, but EKG and serum enzymes remained normal ("preinfarct," crescendo, unstable, or accelerated angina). At this time a cardiac catheterization showed 90% occlusion of the left anterior descending (LAD) coronary artery. On the 17th day after the onset of pain, severe pain recurred together with an abnormal EKG and the patient was taken immediately to the laboratory where a total occlusion of the LAD was now found and he was treated with intracoronary streptokinase. The artery remained open for only a short time, and balloon angioplasty was performed. However, the patient died 12 hours after onset of the last episode of severe pain. A very early acute myocardial infarct was diagnosed at autopsy together with severe coronary atherosclerosis especially of the LAD which had disruption of atherosclerotic plaques and microscopic evidence of embolization.

Correlation of the complete version of the Selvester QRS scoring system with quantitative anatomic findings for multiple left ventricular myocardial infarcts.

The correlation between myocardial infarct size estimated by the complete version of the Selvester QRS scoring system and that documented by pathoanatomic studies has been reported for single anterior, inferior and posterolateral infarcts. Although previous studies described electrocardiographic changes in patients with multiple infarcts, no quantitative documentation of the ability of such changes to estimate the total amount of left ventricular infarction has been reported. This study of 32 patients with anatomically documented multiple infarcts shows a significant correlation between QRS-estimated and anatomically documented sizes (r = 0.44; p = 0.01), which is less than that previously reported for single infarcts in the anterior, inferior and posterolateral locations. Several of the 54 electrocardiographic criteria were never satisfied. Criteria for posterior infarction were seldom present, suggesting "cancellation effect" of coexisting anterior infarction. These results will be the basis for future modification of QRS criteria for estimating myocardial infarct size.

Sensitivity of a set of myocardial infarction screening criteria in patients with anatomically documented single and multiple infarcts.

A subset of 3 screening criteria (Q wave greater than or equal to 30 ms in lead aVF, any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV in lead V2, and R wave greater than or equal to 40 ms in V1) has been proposed to identify single nonacute myocardial infarcts. Cumulatively, these 3 criteria achieved 95% specificity, and 84 and 77% sensitivities for inferior and anterior myocardial infarcts, respectively, among patients identified by coronary angiography and left ventriculography. This study establishes the true sensitivities of the set of screening criteria in 71 patients with anatomically proven single myocardial infarcts and 32 patients with multiple myocardial infarcts. In the single inferior infarct group, the aVF criterion was 90% sensitive. The V2 criterion (any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV) was 67% sensitive in the single anterior infarct group. No single criterion proved sensitive in identifying a posterolateral infarct. The set of screening criteria performed just as well for multiple infarcts as it did for single infarcts, with a cumulative sensitivity of 72%. The overall sensitivity of the screening set in the 103 patients in all groups was 71%.

Anatomic validation of electrocardiographic estimation of the size of acute or healed myocardial infarcts.

Seventeen new criteria added to the simplified version of the Selvester QRS scoring system to comprise the complete version were evaluated to determine their value in estimating the size of single infarcts. These non-Q-wave criteria might be particularly useful regarding posterolateral infarcts in the distribution of the left circumflex artery. The study population was made up of 21 anterior, 30 inferior and 20 posterolateral single myocardial infarction (MI) patients with no evidences of bundle branch or fascicular blocks, ventricular hypertrophy or previous MI on their final stable electrocardiogram. The complete system's maximum 32 points is capable of indicating MI in 96% of the left ventricle and it estimated a mean electrocardiographic MI size that better approximated the anatomic size compared with the simplified version in all MI locations. The correlation between anatomic and electrocardiographic MI size using the complete system was better and statistically significant for the posterolateral MI group (simplified r = 0.55, p less than 0.01 vs complete r = 0.70, p less than 0.0006). Criteria such as Q and S amplitude less than or equal to 0.3 mV in V1 and less than or equal to 0.4 mV in V2 were particularly helpful. This study documents the improved ability provided by the 17 additional non-Q-wave criteria which have been added in the complete version of this scoring system regarding the sizing of infarcts in the region of the left ventricle supplied by the left circumflex artery.

Correlation of clinical history with quantitative histology of lower extremity atheroma biopsies obtained with the Simpson atherectomy catheter.

The purpose of this study was to compare the histologic variability of atheromas resected from patients with various risk factors for vascular disease. Twenty-seven plaques obtained using the Simpson atherectomy catheter were studied. The results of this light and electron microscopic study indicate that patients with diabetes mellitus had increased numbers of smooth muscle cells in their plaques (P less than 0.05) and a trend toward denser, less fatty connective tissue matrix (P less than 0.07) when compared with non-diabetics, and that female diabetics had more smooth muscle cells in their plaques than male diabetics (P less than 0.05). The female patients, regardless of risk factors, had more smooth muscle cells in their plaques than male patients (P less than 0.004). Patients with poor distal runoff had more neovascularization of plaque (P less than 0.001). Tobacco use and age did not have statistically significant correlations with histologic patterns.

Histopathologic examination of material from angioplasty balloon catheters used in vivo in human coronary arteries.

Reports on vascular pathology post-PTCA in both human and animal coronary vessels have revealed medial and intimal cracks and tears, thrombus formation, platelet accumulation, and loss of endothelial cells. The extent and type of damage can currently be assessed in vivo at the macro level by means of coronary artery angiography. However, this technique cannot define vessel wall characteristics at the cellular level. Our hypothesis is that vessel wall material may adhere to the balloon and thus provide a source for coronary artery cytological investigation in vivo. Ten balloon catheters were evaluated to discern any material which was dislodged from the coronary artery and which remained attached to the balloon catheter or guide wire. Our results indicate that angioplasty catheter balloons frequently have adherent collagen, endothelial cells, organized thrombus, and plaque with obvious cholesterol clefts, that can be retrieved and examined histologically. We conclude that material is often dislodged from the plaque during PTCA. In addition, plaque material removed by the balloon catheter offers an unusual opportunity to analyze the morphologic characteristics of cells from the human coronary artery in vivo.

Cryosurgical ablation of atrioventricular nodal reentry: histologic localization of the proximal common pathway.

A method using cryosurgery has been previously described to selectively ablate atrioventricular nodal reentry tachycardia while preserving intact atrioventricular conduction. The purpose of the present study was to define the histologic features of the cryolesions in relationship to the specialized conduction system. In 12 adult dogs a series of nine discrete cryolesions was placed along the perimeter of the triangle of Koch while continuously monitoring the His bundle electrogram. All animals survived the operation and maintained intact atrioventricular conduction. At 14 weeks after surgery the hearts were sectioned and examined. In all 12 animals there was a confluent mass of dense fibrous tissue present in the lower atrial septum that was in immediate proximity to but did not involve the atrioventricular node-His bundle. The ablation of perinodal tissue with preservation of the specialized conduction system with the use of this cryosurgical technique was confirmed. It is likely that the cryoablated perinodal tissue represents the proximal common pathway of the circuit for atrioventricular nodal reentry tachycardia.

Pathology of primary congenital complete heart block.

Studies were done on the hearts of 4 infants and 2 adults with the clinical diagnosis of congenital complete heart block (CCHB) and on the hearts of 6 control patients of similar age groups but without any significant arrhythmia. All 6 patients with CCHB had absence of the fibers [approaches to atrioventricular node (AVN)] connecting the atrium and the AVN and common bundle (CB), as well as having partial or complete absence of the AVN. The mothers of 2 of the 4 infants with CCHB had antibodies to Ro antigen, and one mother (with Ro antibody) had evidence of having had active systemic lupus erythematosus (SLE). One infant developed SLE before the age of 1 yr. In one of the 2 adult cases with CCHB, the patient had evidence of having developed his CHB after birth, and the other adult patient probably had his CCHB since birth. It was suggested that these findings--and others in the literature--could be explained by there being two factors that lead to the occurrence of idiopathic heart block, whether it be truly congenital or acquired later in life: (a) a genetic predisposition to the condition together with (b) a precipitating injury. Thus, a patient with a genetic predisposition to insults to his conducting fibers might develop CCHB in utero due to some insult (e.g., due to damage by circulating anti-DNA antibodies in patients with SLE or by other unknown insults); or the "weak" fibers could be affected later in life by many different injuries--whether viral, hypersensitivity, anoxic, or due to aging.

Comparison of patients with acute anterior or posterior myocardial infarcts with and without complete heart block.

The differences between myocardial infarct (MI) size, amount, and type of conduction fiber injury and outcome in patients with acute anterior or posterior (inferior) MI with or without complete heart block (CHB) were compared. In patients with acute anterior MIs with CHB the infarcts were larger, CHB was more persistent, necrosis involved the more anterior portions of the conduction system, and the terminal event was cardiogenic shock; whereas in the smaller acute posterior MIs with CHB, the CHB was usually transient, necrosis involved the more posterior portions of the conduction system, and terminal arrhythmias were the main cause of death. This is the first quantitative study that documents the larger size of anterior infarcts with complete heart block in comparison with posterior infarcts with complete heart block.

Prognostic implications of an early peak in plasma MB creatine kinase in patients with acute myocardial infarction.

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)