Summary:Hospital records of 120 patients undergoing aortic valve replacement were retrospectively reviewed for risk factors associated with early aortic valve replacement, Patients were separated into four groups (rheumatic, congcnital bicuspid. degenerative, and miscellaneous) based upon the morphologic etiology of aortic stenosis. Multiplc regression analysis was performed using age at surgcry as the dependent variable. lndependent variables for the study were race, gender, systemic hypertension, total triglyceride level, total serum cholesterol level, tobacco smoking history, diabetes mellitus, and angiographic coroiiary artery disease. In the rheumatic valve group only showed a statistically significant risk effect whereas in the congenital bicuspid valve group i u w , g n idcv.? and tri,qIycwicle.s were statistically correlated with age at surgcry. In the degenerative valve group ,qencIcr and .snioAiri,q were found to be statistically significant risk factors. The establishment of aortic stenosis risk factors might be an indication for clinical trials of risk factor modification i n patients with aortic stenosis.
Although various public health preventive efforts and prescribed pharmacologic treatment methods will have long-term benefits in the reduction of coronary artery atherosclerosis and subsequent cardiac events, the immediate and short-term future in the treatment of coronary artery disease will focus on several interventional devices designed to remodel or remove causes of acute and chronic coronary artery obstruction. Certain clinical-morphologic aspects of these interventional devices or techniques that result in remodeling of the coronary lumen shape (balloon angioplasty, thermal probes, intravascular stents) or removal of obstructing material (lasers, atherectomy devices) are reviewed. Two new areas in the pathology of atherosclerotic plaque (plaque fissures, eccentric plaque) and their clinical relevance in coronary heart disease are described.
Dynamic obstruction to left ventricular outflow in patients with hypertrophic cardiomyopathy usually occurs when the anterior mitral leaflet moves forward in systole and approaches or contacts the ventricular septum. However, we have recently identified, by M mode and two-dimensional echocardiography, 21 patients with hypertrophic cardiomyopathy who had a unique pattern of mitral valve motion characterized by abnormal mitral valve coaptation and systolic anterior motion of the posterior mitral leaflet. This abnormality of mitral valve motion was most reliably identified with twodimensional echocardiography in views of the left ventricle obtained from the apex. At end-diastole the anterior and posterior mitral leaflets did not appear to coapt at their distal free margins. Rather, at mitral valve closure, the anterior mitral leaflet contacted the basal portion of posterior mitral leaflet. Subsequently, during systole the "residual" distal portion of posterior mitral leaflet approached or contacted the ventricular septum. Morphologic observations in nine other patients with hypertrophic cardiomyopathy suggested that systolic anterior motion of the posterior mitral leaflet is due to elongation of the middle scallop of the posterior leaflet, which probably comes into apposition with the ventricular septum during systole by passing through the space created by the normal pattern of chordal attachments onto the anterior mitral leaflet. Of the 16 patients who underwent cardiac catheterization, nine had basal subaortic gradients of 20 to 85 mm Hg, which were apparently due to moderate or marked systolic anterior motion of the posterior mitral leaflet. Ventricular septal myotomy-myectomies were performed in two patients and resulted in markedly diminished systolic anterior motion of the posterior mitral leaflet in each and abolition of subaortic gradient in the one patient who underwent postoperative cardiac catheterization. Hence, in patients with hypertrophic cardiomyopathy, systolic anterior motion of the posterior mitral leaflet (1) is not uncommon (identifiable in about 10% of a consecutively studied series of patients), (2) constitutes a previously undescribed mechanism for dynamic subaortic obstruction, and (3) is due to a malformation of the posterior mitral leaflet. Circulation 68, No. 2, 282-293, 1983. A SUBSTANTIAL PROPORTION of patients with hypertrophic cardiomyopathy demonstrate obstruction to left ventricular outflow.'-5 Most available angiographic6' 7 and echocardiographic-25 data appear to indicate that this dynamic subaortic obstruction occurs when the anterior mitral leaflet (AML) (with or without its attached chordae tendineae) approaches or comes into contact with the ventricular septal endocardium. Others have suggested that the chordae tendineae or papillary muscles may primarily produce left
Summary:In the last 15 years, intense interest has focused on various interventional pharmacologic and mechanical forms of therapy for the treatment of atherosclerosis coronary artery disease. Many techniques and devices (dilating balloons, perfusion catheters, thermal probes and balloons, lasers, atherectomy devices, stents, intravascular ultrasound) have been used or are under study for future use. Many of these techniques and devices require an understanding of histologic and pathologic features of the coronary arteries and diseases which affect them. This article reviews selective areas of anatomy, histology, and pathology relevant to the use of various new interventional Part I of this review will focus on anatomic aspects of the epicardial coronary artery system, coronary arterial distribution, myocardial supply, and histologic features of the normal coronary artery.
Key words: coronary artery, coronary ostium, high takeoff position
Epicardial Coronary Artery SystemThe epicardial coronary artery system consists of the left and right coronary arteries, which normally arise from 0s-tia located in the left and right sinuses of Valsalva, respec- tively ( Fig. 1). In about 50% of humans a "third coronary artery" ("conus artery") arises from a separate ostium in the right sinus. Additional smaller ostia may be found in the right sinus, which give rise to multiple right ventricular branches (Fig. 2). Up to five separate coronary ostia have been described (Figs. 2+.3 The left main coronary artery ranges in length from 1-25 mm before bifurcating into the left anterior descending and left circumflex bran~hes.~ The left anterior descending coronary artery measures from 10-13 cm in length, whereas the usual nondominant left circumflex artery measures about 6-8 cm in length. The usual dominant right coronary artery (supplying posterior descending and/or atrioventricular nodal artery) is about 12-14 cm in length before giving rise to the posterior descending artery. The luminal diameters of the major coronary arteries in adults range as follows: left main, 2.0-5.5 mm (mean 4 mm); left anterior descending, 2.0-5.0 mm (mean 3.6 mm); left circumflex, 1.5-5.5 mm (mean 3.0 mm); and right, 1.5-5.5 mm (mean 3.2 mm)? Although the left anterior descending and left circumflex arteries generally taper in diameter as each extends from the left main bifurcation, the right coronary artery maintains a fairly constant diameter until just before the origin of its posterior descending branch. The subepicardial coronary arteries run on the surface of the heart embedded in various amounts of subepicardial fat. Portions of the epicardial coronary arteries may dip into the myocardium ("mural artery" or "tunneled artery") and be covered for a variable length (1 to several mm)5 by ventricular muscle ("myocardial bridge") (
Coronary OstiaThe left and right coronary ostia arise normally within the sinus of Valsalva or at the junction of the sinus and tub-
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