Showing papers in "American Journal of Cardiology in 1980"
TL;DR: Nifedipine is a potent, long-acting vasodilator that has proved highly efficacious in relieving anginal symptoms caused by coronary vasospasm, and its value as an antiarrhythmic agent remains to be delineated.
Abstract: Calcium antagonists (slow channel blocking agents) are a very heterogeneous group of agents with dissimilar structural, electrophysiologic and pharmacologic properties. Nifedipine is a potent, long-acting vasodilator that has proved highly efficacious in relieving anginal symptoms caused by coronary vasospasm. In vivo, it exerts no myocardial depressant effects and has no antiarrhythmic properties. Treatment with nifedipine can safely be combined with administration of a beta receptor blocking agent. VErapamil prolongs atrioventricular (A-V) conduction (A-H interval) in a dose-dependent manner. It is the drug of choice for the treatment of reentrant supraventricular arrhythmias, irrespective of whether reentry occurs within the A-V node or through an accessory pathway (the Wolff-Parkinson-White syndrome). Verapamil is only moderately effective as an antianginal agent. Diltiazem is efficacious for the treatment of angiospastic angina, but its value as an antiarrhythmic agent remains to be delineated.
860 citations
TL;DR: Hearts from the rabbits treated with propranolol, verapamil or nifedipine were protected against ischemia, and ischemIA with reperfusion-induced decline in the ATP-generating and O 2 -utillzing capacity of the mitochondria.
Abstract: To establish whether the prophylactic use of verapamil, nifedipine or propranolol protects heart muscle against the deleterious effects of global ischemia and reperfusion, rabbits were injected subcutaneously twice daily with 2.0 mg/kg of one of these drugs for 4 to 5 days. The hearts were then isolated, paced and either perfused aerobically, made totally ischemic for 90 minutes or made ischemic for 90 minutes and then reperfused. At the end of this time some of the hearts were assayed for adenosine triphosphate (ATP), creatine phosphate (CP) and calcium (Ca ++ ). Other hearts were homogenized, the mitochondria harvested and monitored for oxidative phosphorylating and ATP-generating capacity and Ca ++ content. The effect of Ca ++ on the ATP-generatlng capacity of cardiac mitochondria was also determined. Hearts that were made ischemic gained Ca ++ . The endogenous stores of ATP and CP were depleted; the mitochondria accumulated Ca ++ and the oxidative phosphorylating activity (respiratory control index and oxygen quotient) was impaired. During reperfusion, tissue and mitochondrial Ca ++ was substantially increased, the capacity of the mitochondria to use O 2 for state III respiration was further impaired and the ATP-generating capacity reduced. Resting tension increased and there was only a small recovery of active tension generation. Hearts from the rabbits treated with propranolol, verapamil or nifedipine were protected against ischemia, and ischemia with reperfusion-induced decline in the ATP-generating and O 2 -utillzing capacity of the mitochondria. There was also a less marked increase in tissue and mitochondrial Ca ++ and the systolic tension-generating capacity of the hearts was better maintained.
456 citations
TL;DR: It is indicated that significant prolongation of isovolumic relaxation is seen in different forms of left ventricular hypertrophy and is often associated with an abnormal diastolic filling pattern.
Abstract: To study left ventricular relaxation and filling in different forms of left ventricular hypertrophy, echocardiograms of the left ventricle in 24 patients with hypertrophic obstructive cardiomyopathy and in 24 patients with chronic left ventricular pressure overload (due to aortic stenosis in 6 and to severe arterial hypertension in 18) were analyzed by computer and compared with those of 28 normal subjects. The relaxation time index (minimal left ventricular dimension to mitral valve opening) was 13 ± 15 ms in normal subjects. This index was prolonged in patients with cardiomyopathy (93 ± 37 ms) and overload (66 ± 31 ms). During the interval from minimal left ventricular dimension to mitral valve opening both groups with left ventricular hypertrophy showed a marked increase in left ventricular dimension of 4.0 ± 2.2 mm and 3.0 ±1.8 mm, respectively, which was significantly greater (p The rapid filling phase and the increase in dimension during this period were significantly reduced in hypertrophic obstructive cardiomyopathy and chronic pressure overload. In contrast to findings in the patients with cardiomyopathy, in those with pressure overload the reduced increase in left ventricular dimension during the rapid diastolic filling period was compensated for by a greater dimensional increase due to atrial contraction, resulting in a normal end-diastolic dimension. These data indicate that significant prolongation of isovolumic relaxation is seen in different forms of left ventricular hypertrophy and is often associated with an abnormal diastolic filling pattern.
405 citations
TL;DR: A new palliative procedure for hypoplastic left heart syndrome that has resul;ed in early ongoing survival of two infants with aortic atresia is reported.
Abstract: Aortic atresia is a form of hypoplastic left heart syndrome always complicated by associated severe hypoplasia of the ascending aorta and various degrees of mitral valve and left ventricular hypoplasia. At present it is a universally fatal lesion in early infancy. This is a report of a new palliative procedure for hypoplastic left heart syndrome that has resul;ed in early ongoing survival of two infants with aortic atresia. On the basis of experience with a third patient, an operation for future physiologic correction is proposed.
381 citations
TL;DR: It is concluded that both HDL and LDL cholesterol are strongly and independently associated with the prevalence of coronary heart disease, whereas the level of very low density lipoprotein cholesterol makes no statistically significant independent contribution.
Abstract: Forty-three of 1,312 men aged 35 to 54 years in the Framingham Offspring Study had clinically recognized coronary heart disease at the initial examination. Twenty-six men in this group had previously had a myocardial infarction. Of 1,296 women in the same age range, only 11 had coronary disease and 3 a prior myocardial infarction. The prevalence of coronary heart disease in men was strongly associated with age, smoking, high density lipoprotein (HDL), low density lipoproteln (LDL) and total cholesterol using univariate analyses. When multivariate logistic regression analysis was used, age, smoking and HDL and LDL cholesterol retained their significant association with coronary heart disease. The total cholesterol/HDL cholesterol ratio was also strongly associated with coronary heart disease in the multivariate analysis. It is concluded that both HDL and LDL cholesterol are strongly and independently associated with the prevalence of coronary heart disease, whereas the level of very low density lipoprotein cholesterol makes no statistically significant independent contribution.
327 citations
TL;DR: Good agreement was found between scintigraphic and angiographic determinations ofleft ventricular end-systolic and end-diastolic volumes, and radionuclide techniques, which are independent of geometric assumptions, may be utilized for the quantitation of left ventricular volumes.
Abstract: This study assesses the utility of a scintigraphic, nongeometric technique for the determination of left ventricular volumes. Accordingly, gated blood pool scintigraphy and cineangiography were performed within a 24 hour period in 22 patients. Scintigraphic volume measurements were calculated from individual frames of a modified 35 degrees left anterior oblique projection using an algorithm designed to consider (1) the background-corrected left ventricular activity normalized for activity per milliliter of peripheral venous blood; (2) total study time; (3) number of frames acquired per cardiac cycle; and (4) percent of the cardiac cycle acquired. Angiographic volumes were calculated by the area-length method and the Kennedy regression equation. There was an excellent correlation between scintigraphic and angiographic methods for all volume measurements grouped together (r = 0.985, standard error of the estimate [SEE] = 14.6 ml) as well as for segregated end-diastolic volumes (r = 0.985, SEE = 16.2 ml) and end-systolic volumes (r = 0.988, SEE = 14.7 ml). Prospective testing of the independent ability of scintigraphy to estimate ventricular volumes was provided for by studying an additional 13 patients, and good agreement was found between scintigraphic and angiographic determinations of left ventricular end-systolic and end-diastolic volumes. Thus, radionuclide techniques, which are independent of geometric assumptions, may be utilized for the quantitation of left ventricular volumes.
273 citations
TL;DR: It is concluded that endomyocardial biopsy can be used to diagnose inflammatory myocarditis and to monitor the histologic results of therapy, and circumstantial evidence that immunosuppressive therapy is effective in eliminating myocardial cell inflammation and thereby improvingMyocardial performance is found.
Abstract: Right ventricular endomyocardial biopsy was performed to make a diagnosis of inflammatory myocarditis in 10 patients with congestive heart failure. All 10 patients were treated with immunosuppressive agents (either prednisone alone or prednisone in combination with azathioprine) and were followed up prospectively. Each patient had serial invasive and noninvasive assessments of cardiac performance, and 9 of 10 had one or more follow-up endomyocardial biopsies. The course of four patients who showed dramatic improvement in association with immunosuppressive therapy is described in detail. In addition to these four patients, one other had definite improvement and four subjects had stabilization of previously progressive heart failure; the condition of one patient worsened, and he died despite immunosuppression. In the seven patients who had cell inflammation, six underwent a second biopsy after a period of immunosuppressive therapy, and in each case, the inflammatory infiltrate had been eliminated. In two of these patients, signs and symptoms of myocarditis recurred after discontinuation of therapy, and myocardial biopsy confirmed the recrudescence of cell inflammation. Reinstitution of therapy improved symptoms and histologic findings. It is concluded that endomyocardial biopsy can be used to diagnose inflammatory myocarditis and to monitor the histologic results of therapy. Our findings constitute circumstantial evidence that immunosuppressive therapy is effective in eliminating myocardial cell inflammation and thereby improving myocardial performance.
270 citations
TL;DR: The ergonovine maleate test is not benign and may cause severe coronary vasospasm that is unresponsive to sublingual and intravenous nitroglycerin, but may be reversed by intracoronary nitrogoglyin.
Abstract: Recent experience has suggested that the ergonovine maleate test is a safe procedure for the diagnosis of variant angina pectoris, because ergonovine-induced coronary vasospasm has generally been reversible by sublingual nitroglycerin. This report describes five cases of ergonovine-induced coronary vasospasm that were refractory to sublingual nitroglycerin. Four of these patients had cardiac arrest. In two patients the vasospasm was responsive to intracoronary nitroglycerin administration. Three patients died as a result of the test. The two survivors differed from the nonsurvivors in the total dose of ergonovine given (0.1 and 0.15 mg versus 0.17, 0.3 and 0.3 mg, respectively) and in the method of administration of ergonovine. The survivors were given serial doses of 0.05 mg each, whereas the three nonsurvivors received either larger initial doses (0.1 followed by 0.07 mg) or progressive incremental doses (0.05, 0.1 and 0.15 mg serially). Sublingual nitroglycerin, given to all five patients, and intravenous nitroglycerin, given to three of the five, were ineffective in reversing vasospasm. Intracoronary nitroglycerin favorably altered the course of the survivors. Thus, the ergonovine maleate test is not benign and may cause severe coronary vasospasm that is unresponsive to sublingual and intravenous nitroglycerin, but may be reversed by intracoronary nitroglycerin.
251 citations
TL;DR: Calcific deposits occur commonly in bioprostheses implanted in patients of all ages, but are more likely to become severe and clinically significant in children and in young adults than in older patients.
Abstract: Gross, histologic and ultrastructural studies were made of 14 porcine valve bioprostheses that were found to contain calcific deposits at the time of removal either at reoperation (13 patients) or at necropsy (1 patlent). Eleven bioprostheses had been in the mitral position, 1 fn the aortic, 1 in the tricuspid and 1 in a pulmonary condult. The ages of the patients at the time of implantation ranged from 2.5 to 65 years (average 32), and the bioprostheses had been in place from 3 to 94 months (average 39). Analysis of these 14 bioprostheses and review of reports concerning 37 other calcified porcine bioprostheses suggest the following conclusions: (1) Calcific deposits occur commonly in bioprostheses implanted in patients of all ages, but are more likely to become severe and clinically significant in children and in young adults than in older patients. (2) Calcific deposits can lead to prosthetic valve stenosis, because they can limit the mobility of the cusps; however, they can also be associated with prosthetic valve regurgitation. (3) Metabolic disorders that could contribute to bioprosthetic calcification are not identifiable in most patients having calcified prosthetic tissue valves. (4) The two main sites of deposition of calcium phosphate in porcine valve bioprostheses are the connective tissue in the cusps, particularly in the spongiosa, and small thrombi on the surfaces. (5) Calcification of connective tissue first involves the collagen fibrils; calcification of thrombi involves the mitochondria in platelets and leukocytes trapped in the mesh of fibrin. From these two sites, calcific deposits can grow and spread into other areas of the cusps.
240 citations
TL;DR: The validity of transesophageal echocardiography is confirmed and its usefulness in monitoring changes in ventricular function during cardiac surgery is confirmed.
Abstract: Transesophageal M mode echocardiography was used for continuous monitoring of left ventricular dimensions in 21 patients (11 with valvular and 10 with coronary heart disease) undergoing open heart surgery. Echocardiograms were recorded in six stages of the procedure and simultaneous measurements of cardiac output (with dye dilution) and atrial pressures were made. Measurements of left ventricular diameters with the transesophageal technique correlated excellently with the corresponding measurements obtained with the standard parasternal method. In patients with volume overload, surgical correction was accompanied by a decrease in diastolic dimension, velocity of circumferential fiber shortening, mid wall stress and end-diastolic stiffness, and an increase in cardiac output. Pericardial and chest wall closures generally caused a significant decrease in cardiac output, and correlated with a decrease in diastolic diameter and an increase in the stiffness constant of the left ventricle. Thus, the decrease in cardiac output may have been due to decreased distensibility of the ventricular cavity secondary to mechanical restriction by the pericardium and chest wall. Pericardial opening caused a significant delay in septal motion that was reversed by closing the pericardium. This study confirms the validity of transesophageal echocardiography and its usefulness in monitoring changes in ventricular function during cardiac surgery.
226 citations
TL;DR: It is concluded that ventricular tachycardia resembling the clinical variety can be induced in the laboratory in almost all patients with sustained ventricularTachycardIA clinically, in the majority of those with symptomatic nonsustained ventriculartachycardie clinically, and only rarely in patients with no previously documented ventricular gyrations.
Abstract: Five hundred twenty-nine patients were studied with programmed ventricular stimulation for evaluation of supraventricular and ventricular tachyarrhythmias. Eighty-six patients had clinical ventricular tachycardia. Sustained ventricular tachycardia was induced in 52 (91 percent) of the 57 patients with a sustained form of the arrhythmia clinically. Nonsustained ventricular tachycardia was induced in 18 (62 percent) of 29 patients with a symptomatic nonsustained form clinically, in 2 (4 percent) of 57 patients with a sustained form and in 3 (0.7 percent) of the 443 patients with no documented spontaneous ventricular tachycardia. Ventricular tachycardia (sustained or nonsustained) was induced by double right or left ventricular extrastimuli in 47 patients (63 percent) and by single right ventricular extrastimuli in 23 (31 percent); in 5 (7 percent), it was inducible only by rapid ventricular pacing and in 9 (12 percent) only by left ventricular stimulation. All 52 patients with induced sustained ventricular tachycardia had the sustained form clinically. Of the 23 patients with induced nonsustained ventricular tachycardia, 18 (78 percent) had the nonsustained form clinically. Four hundred fifty-four patients had no induced ventricular tachycardia; only 14 (3 percent) of these had the arrhythmia spontaneously. The morphologic features, axis and cycle length of 54 of 62 episodes of induced ventricular tachycardia in 43 patients were similar to those of the clinically observed arrhythmia. It is concluded that ventricular tachycardia resembling the clinical variety can be induced in the laboratory in almost all patients with sustained ventricular tachycardia clinically, in the majority of those with symptomatic nonsustained ventricular tachycardia clinically, and only rarely in patients with no previously documented ventricular tachycardia. Conversely, induction of ventricular tachycardia implies the likelihood of spontaneous episodes of this arrhythmia.
TL;DR: Exercise testing identified a small group (1 percent of the total population) who had the highest 5 year probability of primary coronary heart disease (0.33), and four variables obtained from the response to symptom-limited maximal exercise testing were significantly associated with subsequent primary coronaryHeart disease events.
Abstract: Of 2,365 clinically healthy men who participated in the exercise testing unit of the Seattle Heart Watch, follow-up by annual mail questionnaires identified 47 persons (2 percent) who experienced primary coronary heart disease events. The mean follow-up period (± standard deviation) was 5.6 ±1.4 years. The rates of such events was higher in men 55 or more years of age than in the younger men. A count of the conventional risk factors identified at the time of initial examination was associated with increased 5 year probability of primary coronary heart disease events. However, univariate analysis of the individual risk factors (positive family history, hypertension, smoking, hypercholesterolemia) did not show a significant increase in 5 year probability. Four variables obtained from the response to symptom-limited maximal exercise testing were significantly associated with subsequent primary coronary heart disease events. These predictors were chest pain during maximal exertion, duration of exercise less than 6 minutes with the Bruce protocol, failure to attain at least 90 percent of the age-predicted maximal heart rate and ischemie S-T segment depression. When the conventional risk factors and the exercise predictors are both considered in asymptomatic men, maximal exercise testing identified a small group (1 percent of the total population) who had the highest 5 year probability of primary coronary heart disease (0.33). This group had one or more conventional risk factors and two or more exercise predictors identified. The probability in those with conventional risk factors but with less than two exercise predictors was 0.015. Forty-one percent of the population had no risk factors and the 5 year probability in this group was 0.01. Exercise testing was of no predictive value in the latter group.
TL;DR: Measurements of normal portions of "spastic" and "nonspastic" vessels suggested a generalized uniform constriction of all major coronary arteries during attacks, with "spasm" limited to the site of an organic lesion in most cases.
Abstract: Coronary arterial spasm is a problem of older adults; it has not to my knowledge been described in children. This suggests that a prerequisite is a coronary artery which has acquired an abnormality as it has aged. Variant angina is a condition most commonly due to large coronary artery spasm. In the 80 patients I have personally seen with it, angiographically detectable disease was present in the vessel involved with spasm in 95% of cases. Careful study of cases presented in the literature as having ‘normal’ coronary arteries actually reveals in many instances minor, persistent irregularities in the vessel which goes into spasm.
TL;DR: The left ventricular response to volume loading and graded supine bicycle exercise was assessed in nine long-term cardiac transplant recipients and plasma norepinephrine was measured by radio-enzymatic assay at each level of exercise.
Abstract: The left ventricular response to volume loading and graded supine bicycle exercise (3 minutes at 15, 45 and 90 watts) was assessed in nine long-term (more than 1 year) cardiac transplant recipients. Computer-aided fluoroscopy of radiopaque myocardial markers implanted in the left ventricle at the time of surgery was used to measure left ventricular dynamics. Pulmonary arterial and left ventricular pressures were monitored. Plasma norepinephrine was measured by radio-enzymatic assay at each level of exercise. Early in exercise mean end-diastolic volume (six patients) increased from a resting value of 125 to 138 ml (p
TL;DR: The data currently available suggest that the vast majority of patients fulfilling the basic anatomic criteria for hypertrophic cardiomyopathy have a distinct disease entity with diverse clinical manifestations.
Abstract: Neither asymmetric septal hypertrophy (ASH), marked cell disorganization in the ventricular septum nor systolic anterior motion of the anterior mitral leaflet (SAM) is pathognomonic of hypertrophic Cardiomyopathy. However, each is uncommonly found in patients with other cardiac disorders and is therefore a highly specific hallmark of hypertrophic cardiomyopathy. Disproportionate septal thickening does occur in about 10 percent of older children and adults with various acquired or congenital heart diseases. In these patients it usually appears to be secondary to the underlying hemodynamic state. However, disproportionate septal thickening is the usual finding in the developing embryonic and fetal heart and it is relatively common (prevalence rate about 25 percent) in normal neonates and infants with congenital heart disease. Likewise, although cell disorganization in the ventricular septum may occur with other cardiac malformations, extensive disorganization is present in about 90 percent of patients with hypertrophic cardiomyopathy and in only about 5 percent of patients with other cardiac diseases. Finally, systolic anterior motion of the anterior mitral leaflet is characteristic of those patients with hypertrophic cardiomyopathy who have obstruction to left ventricular outflow, and it rarely appears (prevalence rate about 3 percent) under basal conditions in other hemodynamic states or cardiac diseases. Hence, in analyses comprising over 1,600 patients the specificity of asymmetric septal hypertrophy, marked septal disorganization and systolic anterior motion of the anterior mitral leaflet was at least 90 percent (90, 93 and 97 percent, respectively). Furthermore, the sensitivity of extensive septal disorganization for hypertrophic cardiomyopathy was 90 percent. The data currently available therefore suggest that the vast majority of patients fulfilling the basic anatomic criteria for hypertrophic cardiomyopathy (that is, a hypertrophied nondilated left ventricle in the absence of a cardiac or systemic disease that itself could produce left ventricular hypertrophy) have a distinct disease entity with diverse clinical manifestations. The majority of such patients appear to have a genetically transmitted disease, but it is not known precisely what proportion of these patients have phenotypically similar but etiologically separate disease entities.
TL;DR: Increased lung activity was related to a greater number of myocardial segmental thallium defects and moderate activity in the lungs but less intense than that in left ventricular myocardium.
Abstract: To determine the clinical significance of increased thallium-201 activity in the lung immediately after exercise stress, the thallium-201 scans in 227 patients undergoing cardiac catheterization were reviewed. Thallium lung activity on the Initial anterior view images were graded qualitatively as follows: 0 (none) in 175 patients (77 percent); 1+ (moderate—increased activity in the lungs but less intense than that in left ventricular myocardium) in 37 patients (16 percent); and 2+ (severe—activity equal to or greater in intensity than left ventricular myocardlal activity) in 15 patients (7 percent). Increased (1+ or 2+) lung activity was related to (1) a greater number of myocardial segmental thallium defects (probability [p]
TL;DR: Most late deaths and complicatins appeared within 2 years of operation, and accelerating deterioration in late results did not occur as the follow-up extended beyond 2 decades.
Abstract: Four hundred seventy-five patients underwent repair of tetralogy of Fallot from 1955 to 1964; 396 of these were hospital survivors and were followed up for 12 to 22 years. An excellent late clinical result was maintained by 87 percent of the 396 hospital survivors. A less than excellent result in the remaining 13 percent of hospital survivors was caused by late mortality in 7 percent (sudden death in 3 percent, death due to cardiac causes in 2 percent and death due to noncardiac causes in 2 percent), required reoperation in 4 percent (mainly because of residual ventricular septal defect) and development of symptoms in 2 percent. Postoperative cardiomegaly (cardiothoracic ratio greater than 0.55) was observed in 60 (25 percent) of 246 patients who had a follow-up chest roentgenogram, and was more common among those who died late or remained symptomatic. Among the few patients with inadequate surgical relief of right ventricular hypertension who did not have transanular patch repair, the hypertension did not tend to decrease progressively, whereas it did decrease in patients who had patch repair. No late sudden deaths were encountered in 20 patients shown to have postoperative right bundle branch block plus left axis deviation (bifascicular block pattern). Pulmonary valve incompetence appeared to have relatively little harmful influence on the late result, causing cardiac disability in 1 percent of the patients and appeared to be the main contributing factor of postoperative cardiomegaly in 13 (5 percent) of the 246 patients who had a follow-up chest roentgenogram. Most late deaths and complications appeared within 2 years of operation, and accelerating deterioration in late results did not occur as the follow-up extended beyond 2 decades.
TL;DR: Programmed atrial stimulation and atrial endocardial mapping were used to analyze the substrate of atrial conduction as well as the mode of initiation and termination of flutter, finding that failure to terminate flutter was associated with local areas ofatrial fibrillation in one or more intracardiac leads.
Abstract: Forty-one of 525 consecutively studied patients had sustained (2 or more minutes) atrial flutter in response to programmed atrial simulation. Of these 41 patients, 31 had previously documented spontaneous atrial flutter or fibrillation, or both, and 10 had paroxysmal palpitations without documentation of the cause. Programmed atrial stimulation and atrial endocardial mapping were used to analyze the substrate of atrial conduction as well as the mode of initiation and termination of flutter. Atrial conduction defects were present in 36 of the 41 patients. Atrial flutter was induced by one or two atrial extrastimuli in 31 patients. In most of these patients the onset of flutter was characterized by a brief period of irregular atrial activity in one or more intracardial leads. Stimulation from the high right atrium was more successful (29 of 31 patients) than that from the coronary sinus (6 of 12 patients). Rapid atrial pacing at cycle lengths of 350 to 200 ms initiated flutter in 29 of 35 patients in whom it was attempted (in 27 of 35 from the high right atrium and in 10 of 18 from the coronary sinus). Termination of flutter was accomplished by rapid pacing in 34 patients at cycle lengths 20 to 55 ms less than the flutter cycle length. Failure to terminate flutter was associated with local areas of atrial fibrillation in one or more intracardiac leads.
TL;DR: The diagnostic accuracy and clinical utility of these two tests for the detection of coronary artery disease are compared and the strengths and weaknesses of each approach are discussed.
Abstract: Exercise thallium-201 myocardial imaging and exercise radionuclide angiography are the two techniques of nuclear cardiology most widely used for the diagnosis of coronary artery disease. Each of these tests provides information of diagnostic and functional value. The diagnostic accuracy and clinical utility of these two tests for the detection of coronary artery disease are compared. The strengths and weaknesses of each approach are discussed. A clinical approach to the detection and evaluation of coronary artery disease using these radionuclide exercise techniques is presented.
TL;DR: The purpose of the present study was to examine whether the impaired left ventricular relaxation in patients with obstructive and nonobstructive hypertrophic cardiomyopathy can be improved by intravenous application of verapamil.
Abstract: Hypertrophic obstructive and nonobstructive cardiomyopathy are often associated with an abnormal prolonged left ventricular isovolumic relaxation time and a disturbed left ventricular filling pattern [1–5]. Recent experimental studies revealed that calcium antagonists may improve impaired left ventricular relaxation caused by ischemia or hypoxia [6, 7]. Based on these experimental results, it was the purpose of the present study to examine whether the impaired left ventricular relaxation in patients with obstructive and nonobstructive hypertrophic cardiomyopathy can be improved by intravenous application of verapamil.
TL;DR: Patients with uncomplicated myocardial infarction who are at risk for a future cardiac event are identified by identifying S-T segment depression, angina pectoris or an inadequate blood pressure response during modified treadmill exercise testing before hospital discharge.
Abstract: Recently, modified treadmill exercise testing before hospital discharge has been reported to be safe in patients after uncomplicated myocardial infarction. Accordingly, the frequency of treadmill exercise-induced abnormalities and their prognostic value were evaluated in 130 patients with uncomplicated myocardlal infarction. Seventy-eight patients (60 percent) had one or more treadmill exercise-induced abnormalities; 42 had S-T segment depression, 35 had angina and 17 had an inadequate blood pressure response. During the mean follow-up period of 11 months, 27 patients experienced unstable angina, 12 had a recurrent myocardlal infarction and 10 died of cardiac causes. Compared with patients with no exercise-induced abnormality, patients with S-T segment depression, angina pectoris or an inadequate blood pressure response had a significantly greater (p
TL;DR: Patients who do not experience it during myocardial ischemia--or whose symptoms are so trivial as to be disregarded--may be thought of as having a defective anginal warning system.
Abstract: The syndrome of silent myocardial ischemia is a subject of continuing controversy. Although some physicians doubt that it is possible to have myocardial ischemia without anginal symptoms, most physicians believe it occurs but are unsure of its prevalence and clinical significance. Because angina may be regarded as a warning to stop an activity before there is further potentially fatal damage to the myocardium, patients who do not experience it during myocardial ischemia--or whose symptoms are so trivial as to be disregarded--may be thought of as having a defective anginal warning system. The defect may be considered incomplete in patients whose ischemic episodes are occasionally symptomatic and complete in patients who never experience angina. In discussing this syndrome, two assumptions need to be made. The first assumption is that there are objective indicators of myocardial ischemia that can be evaluated in clinical studies and correlated with the presence or absence of symptoms. This assumption appears valid. Generally accepted indicators of myocardial ischemia include stress-induced abnormalities of left ventricular wall motion, myocardial perfusion and lactate metabolism in regions subserved by stenosed coronary arteries. In the absence of symptoms, there is perhaps less agreement concerning the reliability of certain electrocardiographic indicators of myocardial ischemia such as S-T segment abnormalities and ventricular arrhythmias. The second assumption is that the history taken accurately reflects the absence of angina pectoris or its usual equivalents in the particular patient. The validity of this second assumption rests
TL;DR: Real time two dimensional echocardiography is useful in differentiating pseudoaneurysm from true aneurysm of the left ventricle, and this finding produced a characteristic beak-like configuration in the studies of two patients.
Abstract: Real time two dimensional echocardiographic findings in four patients with a pathologically proved left ventricular pseudoaneurysm were compared with those in seven patients with a similarly proved true aneurysm of the left ventricle. Pseudoaneurysms produced a bounded echo-free space with a narrow neck that communicated with the left ventricular cavity. The maximal internal width of this neck (O max ) was much smaller than the maximal parallel internal diameter (D max ) of the aneurysmal sac, and the ratio O max /D max never exceeded 0.5. In all cases the pseudoaneurysm could be seen extending behind the intact portion of the involved left ventricular wall, and this finding produced a characteristic beak-like configuration in the studies of two patients. In contrast, true aneurysm resulted in local bulging and dilatation of the left ventricular wall so that the maximal internal width of the mouth (O max ) was nearly equal to, or actually represented, the maximal internal diameter (D max ) of the aneurysm so that the ratio O max /D max ranged from 0.9 to 1.0. Our preliminary study indicates that real time two dimensional echocardiography is useful in differentiating pseudoaneurysm from true aneurysm of the left ventricle.
TL;DR: It is concluded that sustained ventricular tachycardia after repair of tetralogy of Fallot in four patients was caused by reentry at the site of the previous operation in the right ventricular outflow tract.
Abstract: The electrophysiologic characteristics of sustained ventricular tachycardia occurring after total repair of tetralogy of Fallot are reported. Four patients, 8 to 31 years of age, who had spontaneous episodes of sustained ventricular tachycardia underwent electrophysiologic study to determine the mechanism and site of origin of the tachycardia. In each patient, the tachycardia could be reproducibly initiated and terminated by programmed electrical stimulation. In two patients, initiation and maintenance of the tachycardia depended on the development and perpetuation of continuous electrical activity in the right ventricular outflow tract. These observations suggested a reentrant mechanism. In each patient, catheter endocardial mapping demonstrated the site of origin to be the right ventricular outflow tract. In two patients intraoperative mapping showed the reentrant circuit originating at the site of healed right ventriculotomy site. We conclude that sustained ventricular tachycardia after repair of tetralogy of Fallot in our patients was caused by reentry at the site of the previous operation in the right ventricular outflow tract.
TL;DR: To determine why exercise testing remains controversial as a diagnostic test for coronary artery disease, a methodologic review was undertaken of 33 studies comprising 7,501 patients who had undergone both exercise tests and coronary angiography.
Abstract: To determine why exercise testing remains controversial as a diagnostic test for coronary artery disease, a methodologic review was undertaken of 33 studies comprising 7,501 patients who had undergone both exercise tests and coronary angiography. Of seven methodologic standards for research design, only one received general compliance: the requirement for an adequate variety of anatomic lesions. Less than half of the studies complied with any of the remaining six standards: adequate identification of the groups selected for study; adequate analysis for relevant chest paln syndromes; avoidance of a limited challenge group; and avoidance of work-up bias, diagnostic review bias and test review bias. Only one study met as many as five standards. These methodologic problems may explain the wide range of sensitivity (35 to 88 percent) and specificity (41 to 100 percent) found for exercise testing, because the variations could not be attributed to the usual explanations: definition of anatomic abnormality, stress test technique or definition of an abnormal test. Determining the true value of exercise testing requires methodologic improvements in patient selection, data collection and data analysis.
TL;DR: There is evidence that repeated administration of prazosin to patients with severe congestive heart failure results in tolerance to its initial salutary effects as a vasodilator.
Abstract: There is evidence that repeated administration of prazosin to patients with severe congestive heart failure results in tolerance to its initial salutary effects as a vasodilator. Therefore, we used a randomized, double blind protocol to evaluate the clinical effectiveness of 2 months of continuous prazosin therapy in 22 patients with severe congestive heart failure. After 2 months, the patients treated with prazosin showed significant improvement in mean New York Heart Association functional class (3.7 ± 0.2 to 2.3 ± 0.2, p
TL;DR: Evidence of enhanced sympathetic activity during surgery may be a useful predictor of the development of postoperative hypertension, particularly in patients with a longer history of angina of greater severity.
Abstract: A prospective study of hypertension first appearing during and after saphenous vein bypass coronary surgery was performed in 28 patients to examine the incidence, hemodynamics and mechanism of this problem In 15 patients (54 percent) new hypertension developed (mean arterial pressure greater than 107 mm Hg), characterized by increased peripheral vascular resistance and unchanged cardiac output within 1 hour after surgery These 15 patients had a longer history of angina of greater severity, but also had relatively well preserved ventricular myocardium Because plasma renin activity was depressed in patients in the hypertensive group, activation of the renin-angiotensin system was not important in the pathogenesis of this postoperative hypertension The expected decrease in total peripheral resistance at the onset of cardiopulmonary bypass was observed in all patients, but later during bypass the peripheral resistance increased in all patients in association with a rise in plasma epinephrine levels Patients who had hypertension postoperatively had a greater increase in arterial pressure and total peripheral resistance during cardiopulmonary bypass than did those with normal postoperative blood pressure An elevation in plasma epinephrine and norepinephrine concentration, suggesting enhanced sympathoadrenal responsiveness to the challenge of cardiopulmonary bypass, was characteristic of the hypertensive group This evidence of enhanced sympathetic activity during surgery may be a useful predictor of the development of postoperative hypertension
TL;DR: Clinical and necropsy observations are described in five white male runners who ran 22 to 176 km/week for 1 to 10 years, and all died while running, with coronary heart disease appearing to be the major killer of conditioned runners aged 40 years and over.
Abstract: Clinical and necropsy observations are described in five white male runners aged 40 to 53 years (average 46 years) who ran 22 to 176 km/week (mean 53 km) for 1 to 10 years (mean 5). None had clinical evidence of cardiac disease before they became habitual runners, and all died while running. At necropsy all had severe atherosclerotic luminal narrowing of their major epicardial coronary arteries. Of the five runners, at least four had hypercholesterolemia, two had systemic hypertension, one had angina pectoris and none had clinical evidence of an acute myocardial infarct. The single symptomatic runner also had an abnormal resting electrocardiogram and a positive exercise stress test. The electrocardiogram (four patients) and exercise stress tests (three patients) in the other four runners were normal. At autopsy, all five men had greater than 75 percent narrowing of cross-sectional area by atherosclerotic plaques of the right, left anterior descending and left circumflex coronary arteries. In three men the entire lengths of these three coronary arteries and also the left main coronary artery were examined histologically ( total 5 mm segments = 153); 73 (48 percent) of the segments were narrowed greater than 75 percent in cross-sectional area by atherosclerotic plaques and 32 (21 percent) were narrowed by 51 to 75 percent. Four of the five runners had healed (clinically silent) myocardial infarcts. Thus, coronary heart disease appears to be the major killer of conditioned runners aged 40 years and over who die while running.
TL;DR: It is suggested that ventricular tachycardia often precipitates cardiac arrest and electrophysiologic testing may provide data on which to base therapy in patients resuscitated from cardiac arrest.
Abstract: Fifty-two patients resuscitated from cardiac arrest underwent electrophysiologic studies. The earliest documented arrhythmia at the time of initial or recurrent (18 patients) cardiac arrest was ventricular fibrillation (30 patients) or ventricular tachycardia (20 patients); in 2 patients no arrhythmia was documented before defibrillation. Programmed ventricular stimulation revealed inducible arrhythmias in 33 patients (63 percent). Of the 30 patients with ventricular fibrillation as the initial arrhythmia, 13 had inducible arrhythmias—ventricular fibrillation (4 patients), sustained ventricular tachycardia (6 patients) and nonsustained ventricular tachycardia (3 patients). In the 20 patients with ventricular tachycardia as the initial arrhythmia, sustained ventricular tachycardia was initiated in 17 patients and torsade de pointes in 1. Patients with inducible arrhythmias had longer mean A-H and H-V intervals than those without inducible arrhythmias (91.1 versus 76.6 ms and 62.5 versus 50.3 ms, respectively). Prolonged H-V intervals (17 of 33) and intraventricular conduction defects (18 of 33) were more common in patients with than in those without inducible arrhythmias (4 of 19 and 7 of 19, respectively). Mean cardiac index was lower (2.4 versus 3.9 liters/min per m2), left ventricular end-diastolic pressure higher (17.0 versus 9.4 mm Hg), and ejection fraction lower (36.1 versus 57.2 percent) in the group with inducible arrhythmias than in those in whom no arrhythmia could be induced. These data suggest that (1) ventricular tachycardia often precipitates cardiac arrest; and (2) electrophysiologic testing may provide data on which to base therapy in patients resuscitated from cardiac arrest.
TL;DR: A milieu of anatomic and electrophysiologic heterogeneity is apparently sufficient to predispose to the initiation of sustained reentrant ventricular tachyarrhythmias.
Abstract: Ten healthy adult mongrel dogs were subjected to two stage occlusions of the mid or distal left anterior descending coronary artery modified by a reperfusion stage. In 9 of 10 animals studied at 3 or more days after coronary occlusion, sustained reentrant ventricular tachyarrhythmias could be reproducibly initiated or terminated, or both, using routine methods of programmed electric stimulation. Plunge electrodes were inserted at multiple subepicardial, intramyocardial and subendocardial sites from areas of normal and infarcted myocardium to evaluate electrophysiologic properties of excitability and refractoriness. With use of constant current unipolar cathodal stimulation, strength-interval curves were measured at these sites and correlated with regional histopathologic findings. In this model, infarcts were mottled, with close interspersing of normal and abnormal myocardium. Although excitability thresholds and refractoriness tended to increase within areas of infarction, marked disparities in excitability thresholds, effective and relative refractory periods and duration of relative refractory periods (relative minus effective refractory period) were observed within areas of infarction at sites only 1 to 2 mm apart anatomically. This milieu of anatomic and electrophysiologic heterogeneity is apparently sufficient to predispose to the initiation of sustained reentrant ventricular tachyarrhythmias.