Showing papers in "Texas Heart Institute Journal in 1994"

Transmyocardial laser revascularization. Anatomic evidence of long-term channel patency.

Abstract: Transmyocardial laser revascularization, a new surgical technique, is being tested in patients with chronic obstructive coronary artery disease that is refractory to conventional revascularization techniques and to maximal medical therapy. During the operation, which is performed on the beating heart through a left thoracotomy, a high-energy CO2 laser is used to bore transmural channels (1 mm in diameter) into the left ventricle. Each high-energy laser pulse is delivered during end diastole and transects the heart within 10 to 60 msec. The operation is based on the theory that blood will flow directly from the left ventricle into the channels and then into the myocardial vascular plexus. Restoring perfusion should alleviate ischemia in potentially viable myocardium and improve ventricular function. Recently, one of our patients died 3 months after transmyocardial laser revascularization of causes unrelated to the operation. Histologic analysis enabled us to obtain, for the 1st time, anatomic evidence of patent laser channels. Routine staining of cardiac tissue with hematoxylin and eosin revealed multiple patent channels, running perpendicular to and interconnecting with the native vasculature. Although reactive fibrous scar tissue had caused narrowing of the original laser tract, the channels had endothelialized and they contained red blood cells. These findings suggest that the laser channels were functional. We report this interesting case and briefly discuss the anatomic and physiologic phenomena involved in establishing camerosinusoidal blood flow by use of transmyocardial laser revascularization.

Regulation of smooth muscle cell growth by endothelium-derived factors.

Abstract: The endothelium is a source of molecules that either stimulate or inhibit the proliferation of the underlying smooth muscle cells. In the normal, healthy vessel wall the smooth muscle cells are quiescent, but they proliferate when damage to the endothelium occurs. The implication of such observations is that although the endothelium provides a source of growth factors, their stimulatory activity on smooth muscle cells is countered by endothelium-derived growth inhibitors. The inhibitors appear to comprise at least 3 distinct types of molecules: heparin/heparan sulfate; transforming growth factor beta; and nitric oxide. Each molecule inhibits growth of cultured smooth muscle cells by mechanisms that remain to be elucidated and are discussed in this communication. Heparin/heparan sulfate is the most thoroughly characterized of the 3, and has been used for clinical intervention to prevent restenosis. Transforming growth factor beta exhibits bimodal activity on growth, acting as a stimulant at low levels and as an inhibitor at elevated concentrations. Nitric oxide mediated vasorelaxation is dependent upon activation of soluble guanylate cyclase. Because elevation of cyclic guanosine monophosphate in smooth muscle cells depresses their proliferation, nitric oxide would appear to possess the properties necessary to inhibit vascular smooth muscle cell proliferation.

Primary malignant mesothelioma of the pericardium. Case report and literature review.

Abstract: Pericardial mesothelioma is a highly lethal and fortunately rare cardiac neoplasm. We present the clinical and pathologic features of a primary sarcomatoid mesothelioma. To better understand the clinical, radiographic, and pathologic features of this entity, we reviewed 27 cases described in the English literature from 1972 through 1992, which, together with our case, provided a total of 28 cases. Findings of the review include a male-female ratio of 2:1, a wide age range (12 to 77 years; mean, 47 years), and documented asbestos exposure in 4 of 28 (14%) patients. Commonly used imaging studies do not appear to offer great sensitivity, for a mass was detected by echocardiography in only 2 of 16 (12%) patients and by computed tomography in 4 of 9 (44%). Pathologic findings revealed a diffuse growth pattern in most cases (18 of 25, or 72%), together with an equal distribution between the biphasic, epithelioid, and sarcomatoid variants. Effusion cytology revealed malignant cells in only 2 of 10 (20%) cases. With or without therapy, prognosis was uniformly poor, since 24 of 27 patients were dead of the disease at the time the reports were published.

Neointima formation after acute vascular injury. Role of counteradhesive extracellular matrix proteins.

Abstract: Restenosis currently limits the long-term beneficial effects of balloon coronary angioplasty. Two important cellular events in the development of clinically significant luminal narrowing after angioplasty are 1) increased production of extracellular matrix proteins and 2) acquisition of a motile phenotype by vascular smooth muscle cells. In this paper, smooth muscle cell responses that produce a fibrocellular neointima after acute vascular injury are reviewed. Particular emphasis is placed on specialized extracellular matrix proteins implicated in cell movement and tissue repair. Tenascin and thrombospondin are large, modular extracellular matrix glycoproteins; they possess both adhesive and counteradhesive domains and are expressed at high levels during smooth muscle cell migration and neointima formation after balloon injury to rat carotid artery. The ability of both tenascin and thrombospondin to down-regulate the assembly and activity of focal adhesions (points of cell-extracellular matrix adhesive interactions) may be important in the conversion of stationary, quiescent smooth muscle cells to cells that are able to move and divide within the strongly adhesive vessel wall. Moreover, tenascin is present in the extracellular matrix as a large 6-armed oligomer (a hexabrachion) that contains both cell-binding and matrix protein-binding domains in each of the hexabrachion arms. The large size and multidomain structure of tenascin and thrombospondin suggest that these proteins may be particularly well suited to form a nascent provisional matrix at sites of 1) neointima formation after acute vascular injury, 2) new growth and expansion within primary atherosclerotic plaques, and 3) intimal repair and luminal narrowing in restenosis after angioplasty.

Sternitis and mediastinitis after coronary artery bypass grafting. Analysis of risk factors.

Abstract: As part of a quality control program, we analyzed possible risk factors in the development of sternitis and mediastinitis after coronary artery bypass grafting. From 1 January 1990 through 31 December 1991, 1,368 consecutive coronary artery bypass grafting procedures were performed at our institution, either alone or in combination with other procedures. Twenty-three patients (1.7%) developed sternitis and/or mediastinitis; 7 (30.4%) of these patients died in an early postoperative phase. Univariate analysis revealed the following statistically significant (p < or = 0.05) risk factors: perfusion time, length of stay in operating room of longer than 5 hours 30 minutes, presence at the operation of a certain surgical resident, revision for bleeding, and postoperative mechanical ventilation lasting longer than 72 hours. After multivariate analysis, statistically significant independent risk factors were: diabetes mellitus, recent cigarette-smoking, reoperation, presence of a certain surgical resident at the operation, revision for bleeding, and length of mechanical ventilation of longer than 72 hours. The use of both internal thoracic arteries was not, in this study, shown to be an independent risk factor. We conclude that although the technique of using both internal thoracic arteries for myocardial revascularization carries no extra risk by itself in the development of sternitis or mediastinitis, associated factors such as prolonged stay in the operating room and reoperation could be responsible for a higher frequency of sternitis-mediastinitis in patients who have undergone this procedure. Therefore, it is advisable to use this technique selectively in high-risk patients. Close surveillance and reporting of wound infections is mandatory to detect risk factor related to the surgical staff (such as Staphylococcus aureus dissemination).

Anatomy of the action potential in the heart.

Abstract: The surface electrocardiogram can be simply described as the P, QRS, and T (and U) waves, together with PR and ST segments. However, it is actually the summation of the action potential from the sinoatrial node, the atria, the atrioventricular node, the His-Purkinje system, and the ventricles. Although the action potential can be divided grossly into 5 phases, its characteristics vary in different cardiac tissue. This is because the action potential is the end-result of multiple ion channels, pumps, and exchangers opening and closing in concert, and the properties and distribution of these components can be different from one tissue to another. The ion channels can be activated by changes in the membrane voltage and specific ligands, and can be modulated by factors such as neurotransmitters (e.g., through the G-protein system), the G-proteins directly, or other ions. Only in the last 10 years have investigators been able to use molecular biology techniques to peek into the primary structure of ion channels and to develop more workable models of the channel functions. The primary structure and the putative secondary structure of the ion channels show resemblance among the groups, suggesting that, except for IsK, the development of ion channels started with IK1 and IK(ACh), followed by Ito and IK, and then by INa and ICa. However, limitations still exist in our knowledge of the ion channels and hence of the action potential. This is demonstrated by the lack of effective pharmacologic treatment of cardiac arrhythmias to this date. It is to be hoped that advances in cell electrophysiology, genetic engineering, and molecular imaging techniques will soon end the dark days of antiarrhythmic therapy.

Coronary restenosis and gene therapy.

Abstract: Restenosis continues to limit the efficacy of coronary angioplasty, despite the various mechanical and pharmaceutical interventions that have been employed. The migration, proliferation, and extracellular matrix production by vascular smooth muscle cells are processes integral to restenosis, and sustained local delivery of drugs at high concentration should curtail these vascular responses to balloon angioplasty. Our laboratory and others are exploring the potential of using somatic cell gene therapy to provide such treatment and thereby prevent restenosis. However, conventional methods of gene transfer fail to produce physiologic levels of recombinant protein in vivo. This obstacle might be overcome by using adenoviral vectors to mediate efficient direct gene transfer. Herein we summarize these developments and focus upon our laboratory's progress towards evaluating adenovirus-mediated gene therapy in porcine coronary arteries. Recombinant adenoviruses directing the expression of the beta-galactosidase and luciferase reporter genes were evaluated in cultured coronary vascular smooth muscle cells in vitro and in porcine coronary arteries in vivo. Following percutaneous transluminal gene transfer in vivo, recombinant adenoviruses were shown to produce 70- to 240-fold more reporter protein than that produced by Lipofectin-DNA complexes. Furthermore, the high levels of adenovirus-mediated gene expression were shown to persist for at least 14 days following catheterization. Additional histologic studies will be required to determine the cellular distribution of gene expression and to elucidate potential interactions between adenovirus and the host's immune system, but recombinant adenovirus appears to be a promising vector for evaluating gene therapy against coronary restenosis.

Mechanisms of restenosis.

Abstract: Restenosis after percutaneous transluminal coronary angioplasty remains a problem, which suggests that we still do not fully understand its mechanisms. We review here the current understanding of the cell biology of restenosis, including clinical correlation (risk factors), randomized clinical trials, human histology, animal models, and in vitro studies.

Pseudoaneurysm of the left ventricle

Abstract: Pseudoaneurysm of the left ventricle most often occurs after transmural myocardial infarction but may also follow cardiac operations, trauma, inflammation, or infection. In contrast to patients with true ventricular aneurysm, those with false aneurysm most commonly die of hemorrhage. Review of the reported surgical experience and of our 14 cases confirms that standard chest radiographs with an abnormal cardiac silhouette and rapidly expanding size may alert the physician to this sometimes overlooked diagnosis. Noninvasive tests such as color-flow Doppler echocardiography, 2-dimensional echocardiography, cineangiographic computed tomography, and transesophageal echocardiography allow relatively easy recognition of these apparently rare lesions with increasing frequency. Cardiac catheterization, however, is usually still necessary for a clear picture of the location and anatomy of the aneurysm and the state of the coronary arteries. Finally, a new classification is proposed, consisting of true aneurysm, false aneurysm, pseudo-false aneurysm, and mixed aneurysm.

Mycotic aneurysm of the left anterior descending coronary artery after aortic endocarditis. A case report and brief review of the literature.

Abstract: This report concerns a 29-year-old man with recent Streptococcus viridans endocarditis on a bicuspid aortic valve who was found to have a mycotic aneurysm of the left anterior descending coronary artery and infective erosion and thinning of the posterior wall of the ascending aorta 1.5 to 3.5 cm above the origin of the left coronary artery, a combination of lesions not previously reported. Mycotic aneurysm of the coronary arteries affects less than 1% of patients with infective endocarditis, and there are few reports of the management of these rare lesions. The surgical management of this patient is presented with a brief review of the available literature.

The endothelium in health and disease.

Abstract: The early observations of an apparent anomalous action of acetylcholine on the regulation of vascular tone in vivo and in vitro were found to be a reflection of the intactness of the endothelium in vivo. An intact endothelium mediates relaxation of smooth muscle in response to acetylcholine, whereas endothelium-denuded blood vessels exposed to this agonist often exhibit vasoconstriction. The vasodilation is mediated by the actions of the endothelium-derived relaxing factors nitric oxide and prostacyclin. In addition, endothelial cells release endothelium-derived hyperpolarizing factor, which regulates potassium-channel opening in vascular smooth muscle. The chemical nature of this molecule remains to be elucidated. Many of the physiologic stimulants for endothelium-derived relaxing factor production are released by aggregating platelets, and the significance of the endothelium's vasoprotective role becomes apparent when the mechanisms and consequences of platelet agglutination are studied. Damage to the endothelium, however minor, results in the loss of this protective function and is associated with an impaired response to serotonin of G-protein coupled receptors. In the presence of risk factors such as elevated serum cholesterol, the consequences of an impaired endothelial function are greatly enhanced. Age-related changes in endothelial responsiveness may account for the prevalence of cardiovascular disease in human beings over the age of 30 years.

Simultaneous coronary artery bypass and carotid endarterectomy. Determinants of outcome.

Abstract: From January of 1988 to May of 1993, simultaneous single-stage coronary revascularization and carotid endarterectomy was performed in 33 patients (mean age, 69 years). Thirty-one patients (94%) were in New York Heart Association class III or IV, 15 (46%) had unstable angina, and 7 (21%) were operated on because of evolving myocardial infarction. One or more previous myocardial infarctions were present in 18 patients (54%). Nineteen patients (58%) presented with neurologic symptoms, and 22 (67%) had severe bilateral carotid stenosis. Thirty (91%) had triple-vessel or left main coronary artery disease. Sequential reconstruction of the carotid artery followed by coronary artery bypass grafting was performed in all patients. In 4 cases, additional cardiac procedures were performed. Operative mortality (6%) was cardiac related. Perioperative morbidity included myocardial infarction in 1 patient (3%) and neurologic deficit in 6 (18%), with permanent functional impairment in 2 patients (6%). The stroke rate was higher in the bilateral than in the unilateral carotid stenosis group (22.7% vs 9.1%, p = 0.047). Previously completed stroke influenced the operative outcome (55.6% vs 4.2%, p = 0.003). Low ejection fraction (33.5% +/- 7.5% vs 52.8% +/- 3.5%, p = 0.03) and left main coronary artery disease (36% vs 5%, p = 0.03) also predicted postoperative neurologic complications. During a mean follow-up of 24.6 +/- 3.5 months, 3 patients died. The 5-year life-table survival rate was 85%. Eighty-nine percent of long-term survivors were free of cardiovascular disease symptoms. Our results show that the out come of simultaneous carotid endarterectomy/coronary artery bypass grafting in this high-risk population depends upon the preoperative absence or presence of completed stroke or bilateral carotid stenosis, upon the preoperative ejection fraction, and upon the extent of the left main coronary artery disease.

Molecular and Cellular Cardiology

Abstract: R. B. Kleiman and S. R. Houser of Single Feline RV and LV Myocytes F. C. Tan, D. E. Goll and Y. Otsuka Cat + -Dependent Proteinase from Bovine Cardiac Muscle W. Rouslin Zero-flow Ischemia (Autolysis) in Slow and Fast Heart-rate Hearts S. Miki, M. Ashraf, S. Salka and N. Sperelakis Ultrastructural Alterations Mediated by Oxygen Metabolites S. J. Edwards, S. Rattigan, E. Q. Colquhoun, E. A. Woodcock and M. G. Clark Characterization of a,-Adrenergic Receptors in Perfused Rat Heart S. H. Smith, M. McCaslin, C. Sreenan and S. P. Bishop Two-kidney, One Clip Renal Hypertension Y. S. Choong, J. B. Gavin and L. C. Armiger Function and Energy Metabolism of Rat Heart During Ischaemia and Reperfusion J. E. Rosenthal and R. L. Brown Radical Interventions in Canine Purkinje Fibers G. Kessler-Icekson, H. Schlesinger, J. J. Leger, J. Leger, Y. Braverman and 0. Binah Contractile Properties ISHR CALENDAR Electrophysiologic and Mechanical Properties

Tetralogy of Fallot. The first 300 years.

Abstract: The chronicle of tetralogy of Fallot is part of a dramatic evolution in cardiology, cardiac surgery, and understanding of the developing heart. Many new tools and concepts have evolved since Steno of Denmark first described the defect in 1673, and since Fallot of Marseilles coined the term tetralogy in 1888. Four major eras of progress can be recognized. The 1st, the era of pathologic anatomy, culminated in the publication of Maude Abbott's Atlas of Congenital Cardiac Disease in 1936. The next, the era of clinicophysiology and surgery, was highlighted by the 1st Blalock-Taussig anastomosis in 1944, by open-heart surgery 10 years later, and by a new team approach to cardiology. The 3rd, or infant era, began in the mid 1970s with successful intracardiac repair in infants, the rise of echocardiography, and the introduction of prostaglandin therapy. The current era of cardiac development (beginning in the 1990s) gives hope for early understanding of the molecular basis of tetralogy. Tribute is due to the surgical and medical pioneers, and to the pioneer patients and their families, for revolutionary changes in diagnosis and treatment. The challenge of the next 100 years lies in increased understanding of the molecular biology of the defect and in preserving the blend of humanism, scholarship, and skill that have graced the advances of the past 3 centuries.

Molecular basis of hypertrophic and dilated cardiomyopathy.

Abstract: Hypertrophic cardiomyopathy is a heterogeneous disease with autosomal dominant Mendelian inheritance. In 1989, the 1st locus for hypertrophic cardiomyopathy was mapped to cardiac myosin genes located on chromosome 14q1. Soon, several mutations that cosegregated with inheritance of the disease were identified in the beta-myosin heavy chain gene, or MHY7. More than 30 missense mutations and 1 deletion mutation in the beta-myosin heavy chain gene have since been described. Recently, expression of both the mutant beta-myosin heavy chain mRNA and the mutant protein has been shown in the cardiac and skeletal muscles of individuals with hypertrophic cardiomyopathy. Characterization of the clinical features of beta-myosin heavy chain mutations has shown that certain mutations, such as Arg403Gln and Arg719Trp mutations, are associated with high rate of sudden cardiac death. In addition to the beta-myosin heavy chain gene, 3 new loci for hypertrophic cardiomyopathy have recently been described, but the candidate genes have not yet been identified. Dilated cardiomyopathy can be inherited as an autosomal dominant, autosomal recessive, and X-linked disease. The familial form of dilated cardiomyopathy comprises approximately 20% of the cases of idiopathic cardiomyopathy. Echocardiographic abnormalities such as left ventricular enlargement are present in 10% of asymptomatic relatives. No gene for familial dilated cardiomyopathy has been identified, but linkage studies using polymorphic, short-tandem repeat markers are ongoing. Dilated cardiomyopathy is a common manifestation of Duchenne/Becker muscular dystrophy. Heart failure is a common cause of death in the affected individuals. The gene responsible for this disease is the dystrophin gene located on X chromosome. There have been reports in these patients of several dystrophin-gene deletion mutations, which result in a decrease in the expression of the dystrophin protein in the cardiac and skeletal tissues. X-linked cardiomyopathy, in which the disease is restricted to the heart, has also been linked to the dystrophin gene. Myotonic dystrophy is an autosomal dominant disease that commonly involves the myocardium and the conduction tissue, resulting in conduction defects and heart failure. Sudden cardiac death is the most common cause of mortality in patients with myotonic dystrophy. Recently, the myotonin protein kinase gene located on chromosome 19 was identified as the gene responsible for this disease. Expansion of the number of trinucleotide repeats in the myotonin protein kinase gene results in myotonic dystrophy. Mutations in mitochondrial DNA have been associated with hypertrophic and dilated cardiomyopathy. The inheritance of mitochondrial cardiomyopathy is maternal and the disease is associated with certain systemic disorders.

Circumferential dissection of the ascending aorta with intimal intussusception. Case report and review of the literature.

Abstract: The present report describes an unusual case (apparently the 10th in the world literature) of a type-A aortic dissection with full circumferential detachment of the ascending aortic intima and intussusception thereof into the aortic arch and descending aorta, partly occluding the arch vessels Computed tomographic scanning and 2-dimensional echocardiography failed to detect an intimal flap and a false lumen in the ascending aorta Aortic dissection was visualized by aortography The ascending aorta was surgically repaired and the aortic valve resuspended The pertinent literature is reviewed

Identification of defects in the fibrillin gene and protein in individuals with the Marfan syndrome and related disorders.

Abstract: The Marfan syndrome is an autosomal dominant disorder with pleiotropic manifestations that involve the cardiovascular, ocular, and skeletal systems. Through a number of investigational approaches, the gene encoding for fibrillin, the FBN1 gene on chromosome 15, has been identified as the defective gene causing the Marfan syndrome. Fibrillin is the large glycoprotein with a repetitive domain structure and is a major protein component of microfibrils, a fibrillar system closely associated with elastin in connective tissue. Mutational analysis of defects in the FBN1 gene in patients with the Marfan syndrome has revealed that most mutations are private or unique in an affected individual or family. Analysis of fibrillin protein or gene defects in individuals with related phenotypes has revealed that a perinatal lethal syndrome, termed neonatal Marfan syndrome, is due to FBN1 gene mutations. In addition, fibroblast cell strains from a subset of patients with idiopathic scoliosis have fibrillin protein defects. Last, fibroblasts from calves affected with bovine Marfan syndrome display defects in the fibrillin protein. These studies have wide-ranging implications in the diagnosis, treatment, and prevention of Marfan syndrome and related disorders.

Endothelial-dependent procoagulant and anticoagulant mechanisms. Recent advances in understanding.

Abstract: Modulation of endothelial cell coagulant function is one of a group of changes common to many cytokine-mediated events. Changes that 1) cause migration of leukocytes, 2) increase vascular permeability, and 3) increase the thrombotic potential occur at atherosclerotic arterial branch points, in tumor vasculature, and at sites of inflammation. Regulation of procoagulant activity on the luminal surface of the vessel is crucial and is achieved by presentation of a predominantly anticoagulant surface on the endothelium. Inflammatory mediators can cause a decrease in the expression of the anticoagulant mechanisms and up-regulation of the procoagulant tissue factor. However, under these conditions very little tissue factor is exposed to the blood; instead it is sequestered under the endothelium and presumably becomes exposed only when significant vascular damage is present. Inhibition of intravascular coagulation by factor IXai without impairment of extravascular hemostasis suggests that when tissue factor concentrations are low, the continued generation of factor Xa is dependent on the presence of factor IXa. The demonstration that the blockade of factor IXa is selective for prevention of intravascular thrombus formation suggests a new means for managing intravascular thrombosis without altering the normal hemostatic mechanisms.

Coronary heart disease at altitude.

Abstract: In the past, it has been assumed that some basic physiologic responses to altitude, exposure in coronary patients are comparable to those in normal young subjects. In fact there are similar changes in sympathetic activation, heart rate, and blood pressure early after ascent, with decrements in plasma volume, cardiac output, and stroke volume as acclimatization proceeds. These responses are described, and experience with coronary patients is reviewed. During the 1st 2 to 3 days at altitude, coronary patients are at greatest risk of untoward events. Gradual rather than abrupt ascent, a moderate degree of physical conditioning, early limitation of activity to a level tolerated at low altitude for somewhat less), and attention to blood pressure control all appear to have protective effects. Ascent to moderate altitude appears to entail little risk in coronary patients who are asymptomatic or have moderate exercise tolerance, provided that the above precautions are observed and that activity does not exceed levels at lower altitude. If activity is to be increased, pre-ascent treadmill exercise testing or Holter monitor data secured under conditions comparable to those anticipated at altitude may provide reasonable guidelines. For coronary patients previously evaluated and known to be in a high-risk category, indications for ascent should be examined more critically, and precautionary measures should be more rigorous. Advice for patients with known coronary disease who may desire to trek at very high altitude must involve individual evaluation, and guidelines remain elusive.

Polycythemia and the heart. A review.

Abstract: Thrombosis of the coronary arteries, heart chambers, and great vessels is a complication of polycythemia. Previously, the treatment of coronary thrombosis in the presence of this disease was based on exchange phlebotomy. However, the development of efficient thrombolytic agents, emergency catheterization techniques, and coronary artery bypass surgery may make phlebotomy obsolete.

Surgical techniques for aortic valvuloplasty.

Abstract: Since 1988, reparative techniques have been used at our institution to treat valvular insufficiency in selected patients with aortic valve disease. The limitations of aortic valve replacement are well recognized; it is this knowledge that has motivated us to find out whether a subgroup of patients who have aortic insufficiency might be candidates for preservation of their native aortic valves. This subgroup includes patients who have leaflet prolapse, perforation, or calcification. We describe our methods of patient evaluation and selection, as well as our surgical techniques for both bicuspid and tricuspid aortic valve repair.

Echocardiographic evaluation of anuloplasty rings. Comparison of continuity equation and pressure half-time methods.

Abstract: This study was undertaken to compare pressure half-time and continuity equation methods in the postoperative evaluation of anuloplasty rings. We performed 2-dimensional echocardiography and Doppler studies in 39 patients who had undergone valve repair for mitral regurgitation. In patients with a pressure half-time of 110 msec or more (9/39), there was no significant difference in calculated valve area between the 2 methods (p = 0.696). A significant difference was shown between the 2 methods (p < 0.001) in patients with a half-time less than 110 msec (30/39). When patients were classified according to the type of ring they had received, no significant difference was noted between the 2 groups with regard to peak and mean mitral gradients. In patients placed in subgroups according to half-times of less than 110 msec and half-times of 110 msec or more, no difference was noted between groups in terms of mean mitral gradient, presence of mitral regurgitation, left atrial size, left ventricular function, or heart rate. The continuity equation appears to provide much more homogeneous results in the calculation of valve area in patients who have undergone valvular repair for mitral valve regurgitation.

Left ventricular perforation by a pleural drainage tube. Report of a case with survival.

Abstract: We present a case of survival as a result of surgical intervention after perforation of the left ventricle during the insertion of a pleural drainage tube. Surgical intervention was facilitated by the fact that the drainage tube responsible for the suspected perforation of the cardiac cavity was clamped and fastened, as opposed to withdrawn. The location of the perforation was established by measuring the pressure curve through the drainage tube.

Spontaneous cholesterol embolization. A rarely reported entity.

Abstract: Cholesterol embolization sometimes occurs after invasive procedures involving manipulation of the aorta or its major branches, and less commonly occurs after thrombolytic therapy for acute myocardial infarction. Rarer still is spontaneous cholesterol embolization, a case of which we now report. Our patient experienced peripheral embolization, the origin of which was traced to the infrarenal aortic segment and the common iliac vessels. Aortoiliac reconstruction was successful; we believe that surgical management of this condition should be performed in selected cases.

The cumulative risks of prolapsing mitral valve. 40 years of follow-up.

Abstract: Prolapsing mitral valve is a common cardiac condition, occurring in approximately 16 million people in the United States alone. Primary prolapsing mitral valve may be familial or nonfamilial and may be associated with myxomatous degeneration of the mitral valve leaflets, such as occurs in Marfan syndrome and other connective tissue disorders. Secondary forms may be associated with such entities as rheumatic fever (especially after commissurotomy) and coronary artery disease (in the presence of ruptured chordae tendineae), and with such congenital conditions as interatrial defect and primary cardiomyopathy with outflow tract obstruction. Prolapsing mitral valve is characterized by late systolic murmur, mid-systolic click, or both. Arrhythmias occur in the form of benign premature atrial contraction, premature nodal contraction, and paroxysmal atrial tachycardia. As the patient ages, atrial flutter and atrial fibrillation tend to develop. In some chronic cases, especially those involving atrial fibrillation, systemic emboli may occur. Rare premature ventricular contractions may be largely benign, whereas more frequent premature ventricular contractions may lead to severe arrhythmic complexes such as ventricular tachycardia or ventricular fibrillation. With advancing age, atrioventricular conduction defects of varying degrees or sick sinus syndrome may necessitate a pacemaker installation. About one quarter of prolapsing mitral valve cases progress, with increasing mitral insufficiency and increasing enlargement of the left atrium and left ventricle, which at times leads to congestive heart failure. Coronary artery disease may occur with the severity commensurate with the patient's age group. About three quarters of patients with prolapsing mitral valve syndrome lead normal lives.

Studies on the intrinsic activity (efficacy) of human adrenergic receptors. Co-expression of beta 1 and beta 2 reveals a lower efficacy for the beta 1 receptor.

Abstract: Through co-expression of the human beta 1 and beta 2 adrenergic receptors in a single tester cell (the murine L fibroblast) and through assaying the effect of the beta 1 and beta 2 selective blockers CGP 20712A and ICI 118551 on isoproterenol-stimulated adenylyl cyclase, it is shown that the maximal stimulation achievable with a given cell density of beta 1 adrenergic receptor is less than that obtained with the same density of the beta 2 adrenergic receptor. It is concluded that the efficacy of the 2 receptors differs in that the beta 1 adrenergic receptor has a lower efficacy (or intrinsic activity) than does the beta 2 adrenergic receptor.

A patent internal mammary artery graft decreases the risk of reoperative coronary artery bypass surgery.

Abstract: In order to evaluate the potential risks of a patent internal mammary artery bypass at reoperative coronary artery bypass grafting, we have reviewed the records of 233 consecutive patients undergoing reoperative coronary artery bypass grafting between 1 January 1991 and 31 December 1993, including 209 patients having an occluded mammary graft or no mammary graft (Group I) and 24 patients having a patent mammary graft (Group II). With regard to preoperative patient characteristics, the only significant differences between the groups were: Group II patients had a higher preoperative left ventricular ejection fraction than did Group I patients (63.7% +/- 8.9% vs. 52.1% +/- 10.1%, p < 0.001); and Group II patients had received fewer grafts per patient than had patients in Group I (2.2 +/- 1.1 vs 3.6 +/- 1.4 grafts per patient, p < 0.001). There were no entry injuries to the grafts or to the heart in either of the groups. No perioperative mortality was encountered in Group II, while 11 patients died in Group I (p < 0.05). Group II had a significantly higher incidence of reexploration for post-operative bleeding, whereas Group I had a significantly higher incidence of low postoperative cardiac output. The incidence of all other perioperative complications did not differ between the groups. The results of this study support the use of mammary grafts even in patients who are likely to need repeat coronary artery bypass grafting and certainly does not disqualify such patients from a 2nd operation.

Current methods for circulatory support.

Abstract: Although the concept of artificial circulatory support has existed for almost 200 years, it has only been within the last 4 decades that engineers and physicians have developed mechanical devices that can 1) temporarily support the circulation in a patient until the heart recovers or a new heart can be transplanted, or 2) permanently replace a failed heart. In this paper, we briefly describe the devices and techniques that are in current clinical use and speculate on the use of such devices in the future.

Initial experience of mitral valve replacement with total preservation of both valve leaflets.

Abstract: We compared a series of 7 consecutive patients who underwent mitral valve replacement with preservation of both leaflets to a control group of 97 patients who underwent standard mitral valve replacement at our institution during the same period. Use of inotropic drugs and duration of postoperative intensive care were compared and shown to be markedly reduced in the study group; however, statistical analysis was not applied due to the small number of patients. Comparison of the available pre- and postoperative echocardiographic values showed a decrease in left ventricular end-diastolic and end-systolic diameters in patients with preserved leaflets, particularly in those with mitral regurgitation of degenerative origin.

Dobutamine stress echocardiography in clinical practice with a review of the recent literature.

Abstract: Stress echocardiography has been developed in recent years as an effective noninvasive test for the detection and assessment of coronary artery disease. This method combines exercise with 2-dimensional echocardiography, which can assess regional and global left ventricular function during stress. Dobutamine infusion, a pharmacologic means of producing cardiovascular stress, appears to be an excellent alternative to exercise in echocardiographic studies. Currently, it is reserved for patients who cannot exercise at a meaningful level because of advanced age, physical deconditioning, or other factors. This review evaluates the current clinical application of dobutamine stress echocardiography and compares its efficacy with that of exercise echocardiography and nuclear perfusion imaging.