Citations

Abstract —At the community level, the effect of national programs in increasing hypertension awareness, prevention, treatment, and control is unclear. This study evaluated the degree of detection and control of high blood pressure in a random population-based sample of Olmsted County, Minnesota, residents ≥45 years old, of whom 636 subjects among 1245 eligible residents agreed to participate. Home interview and home and office measurements of blood pressure were used to estimate awareness, treatment, and control rates for hypertension in the community. Mean blood pressures (±SD) were 138/80±20/12 mm Hg for men and 137/76±23/11 mm Hg for women. The overall prevalence of hypertension was 53%. The percentage of subjects with treated and controlled hypertension was 16.6%. Thirty-nine percent of subjects were unaware of their hypertension. Despite clinical trial evidence of reduced morbidity and mortality with antihypertensive therapy, recently reported national data suggest a leveling-off trend for treatment and control of hypertension. This population-based study supports these observations and suggests that at a community level, hypertension awareness and blood pressure control rates are suboptimal, presumably because of decreased attention to the detection and control of hypertension.

Background —Atrial septal aneurysm (ASA) is a putative risk factor for cardioembolism. However, the frequency of ASA in the general population has not been adequately determined. Therefore, the frequency in patients with cerebral ischemic events, compared with the frequency in the general population, is poorly defined. We sought to determine the frequency of ASA in the general population and to compare the frequency of ASA in patients with cerebral ischemic events with the frequency in the general population. Methods and Results —The frequency of ASA in the population was determined in 363 subjects, a sample of the participants in the Stroke Prevention: Assessment of Risk in a Community study (control subjects), and was compared with the frequency in 355 age- and sex-matched patients undergoing transesophageal echocardiography in search of a cardiac source of embolism after a focal cerebral ischemic event. The proportion with ASA was 7.9% in patients versus 2.2% in control subjects ( P =0.002; odds ratio of ASA, 3.65; 95% CI, 1.64 to 8.13, in patients versus control subjects). Patent foramen ovale (PFO) was detected with contrast injections in 56% of subjects with ASA. The presence of ASA predicted the presence of PFO (odds ratio of PFO, 4.57; 95% CI, 2.18 to 9.57, in subjects with versus those without ASA). In 86% of subjects with ASA and cerebral ischemia, transesophageal echocardiography did not detect an alternative source of cardioembolism other than an associated PFO. Conclusions —The prevalence of ASA based on this population-based study is 2.2%. The frequency of ASA is relatively higher in patients evaluated with transesophageal echocardiography after a cerebral ischemic event. ASA is frequently associated with PFO, suggesting paradoxical embolism as a mechanism of cardioembolism. In patients with cerebral ischemia and ASA, ASA (with or without PFO) commonly is the only potential cardioembolic source detected with transesophageal echocardiography.

Background —Atherosclerosis of the thoracic aorta is associated with stroke. The association between hypertension, a major risk factor for stroke, and aortic atherosclerosis has not been determined in the general population. Methods and Results —Transesophageal echocardiography was performed in 581 subjects, a random sample of the Olmsted County (Minnesota) population aged ≥45 years participating in the Stroke Prevention: Assessment of Risk in a Community (SPARC) study. Blood pressure was assessed by multiple office measurements and 24-hour ambulatory blood pressure monitoring. The association between blood pressure variables and aortic atherosclerosis was evaluated by multiple logistic regression, adjusting for other associated variables. Among subjects with atherosclerosis, blood pressure variables associated with complex aortic atherosclerosis (protruding plaques ≥4 mm thick, mobile debris, or ulceration) were determined. Age and smoking history were independently associated with aortic atherosclerosis of any degree ( P ≤0.001) and with complex atherosclerosis ( P =0.002), whereas sex, diabetes mellitus, and body mass index were not. Multiple systolic and pulse pressure variables (office and ambulatory), but none of the diastolic blood pressure variables, were associated with atherosclerosis and complex atherosclerosis, adjusting for age and smoking. Among subjects with atherosclerosis, the odds of complex atherosclerosis increased as ambulatory out-of-bed systolic blood pressure increased (odds ratio 1.43 per 10 mm Hg increase, 95% CI 1.10 to 1.87) and with hypertension treatment, adjusting for age and smoking history. Conclusions —High blood pressure is independently associated with aortic atherosclerosis. Among subjects with atherosclerosis, high blood pressure is associated with complex atherosclerosis.

Some, but not all, cardiac arrhythmias are related to pathologic lesions of the cardiac conduction system. Common atrial dysrhythmias and first-degree atrioventricular (A-V) block rarely are explained on the basis of anatomic lesions in specific sites of the conduction system or its blood supply. Second-degree A-V block of Mobitz type II, which may be a precursor of complete (third-degree) heart block, commonly is associated with fibrotic lesions of uncertain etiology in the branching part of the bundle of His or the bundle branches. Ischemic lesions are found less often, and other pathologic processes rarely are present. Chronic complete heart block most often results from nonspecific, fibrotic interruption of the distal bundle of His, or of the first parts of the bundle branches after their origins. Ischemic lesions are uncommonly the cause of chronic block. High-grade A-V block complicating acute myocardial infarction may be associated with infarction of the A-V conduction system, but often morphologic evidence of ischemia cannot be identified. Congenital variants in anatomy of the conduction system are responsible for some relatively uncommon arrhythmias.

One hundred sixty-nine patients underwent replacement of the aortic valve with an aortic valve homograft; of these patients 17 had concomitant commissurotomy or annuloplasty for an associated mitral valve lesion. Homografts were prepared by sterilization with beta-propiolactone solution and stored in Hanks' solution, or were prepared by sterilization with irradiation and stored at -70 C. Operative mortality was 5.3%. Thirty (19%) of the 160 surviving patients had an aortic diastolic murmur at the time of hospital dismissal, and five of these patients had hemodynamically significant homograft incompetence. For 156 patients, follow-up was longer than 6 months; among the 147 patients who survived operation, there were 12 late deaths. Eighty-four per cent (132) of these 156 patients were alive and well 6 to 54 months after operation. Six patients have required reoperation for valve incompetence. An aortic diastolic murmur was present in 43% of patients. Five patients had significant valve incompetence; four of these patients are markedly improved over their preoperative status. Thromboembolism has been a rare complication despite the fact that anticoagulant therapy was not used. Late calcification of the homograft valve has been noted in only one patient.

Serial histologic sections of the atrioventricular (A-V) conduction system were studied in four hearts with persistent common A-V canal, and the anatomic findings were related to the abnormal ECG patterns. Two hearts were examples of the partial form and two of the complete form of A-V canal. The major anatomic abnormalities were: (1) postero-inferior displacement of the A-V node; (2) relatively short distances between the A-V node and the origin of the left bundle branching; (3) marked posteroinferior displacement of the left bundle branching system; and (4) relative hypoplasia of the anterior (superior) left bundle branches. The anatomic configuration of the A-V conduction system in A-V canal could result in relatively early impulse propagation to the posterior aspect of the ventricular septum as suggested by reported electrophysiologica studies. The anatomic findings are considered to be related closely to the known ECG patterns of A-V canal.

The morphology of the atrioventricular (A-V) conduction system was studied by serial histologic section in two cases of tricuspid atresia type IB (without transposition of the great arteries, with subpulmonary stenosis). The A-V node was adjacent to the central fibrous body, and its location was indicated by a "dimple" in the floor of the right atrium. The left bundle branches originated unusually close to the nodal-bundle junction. The right bundle branch was markedly elongated in its course to the right septal endocardium. It was situated along the inferior aspect of the channel-like ventricular septal defect as it traversed the septum. The early origin of the left bundle branches and the markedly elongated course of the right bundle branch were such that, theoretically, abnormal spread of the activation wave might result.

Obstructive pulmonary vascular disease (PVD) was evaluated in lung sections taken at autopsy in 53 patients with complete transposition of the great arteries. Twentythree had intact ventricular septa and 30 had ventricular septal defects. Children of similar age and associated defects had widely differing degrees of PVD and presented a spectrum of disease. In a small number of patients, the presence of pulmonic stenosis (congenital or acquired by pulmonary artery banding in infancy), a small ventricular septal defect, or a large atrial septal defect was not protective against the development of severe PVD. The findings of this study demonstrate the need for thorough hemodynamic evaluation of patients with complete transposition of the great arteries prior to repair by present technics. In addition, operation should probably be performed as soon as technically feasible.

Fourteen hearts with tricuspid atresia were reviewed at autopsy. The study included examples of normally related great arteries and of transposition of the great arteries; instances of pulmonary stenosis were present in both groups. In these examples of tricuspid atresia the size of the right ventricle depended on the size of the ventricular septal defect. The ventricular septal defect and the right ventricle usually were smaller in proportion to the size of the heart in specimens with normally related great arteries. In the absence of transposition of the great arteries, the ventricular septal defect was found to be the site of obstruction to pulmonary flow, and its size in relation to the size of the aorta determined the size of the pulmonary artery. Morphologic abnormalities exist in the region in which the proximal portions of the major atrioventricular conduction system (A-V node, bundle of His, origin of bundle branches) normally are located; thus, anatomic abnormalities in the course of the atrioventricular conduction tissue could be expected in tricuspid atresia. Based on histologic evidence, severe elevation of pulmonary vascular resistance, in general, does not occur in infancy in tricuspid atresia.