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Background-In vivo studies with intravascular ultrasound have shown that complex plaque anatomy and plaque rupture are more frequent in the presence of marked outward remodeling. A large lipid core and a high macrophage count are recognized histological markers for plaque vulnerability. The link between plaque vulnerability in terms of these markers and remodeling in coronary arteries has not been explored. Methods and Results-In 88 male subjects who died suddenly with coronary artery disease, 108 plaques were studied. The percent remodeling was calculated. Lesions with remodeling Ն0% were considered to have positive remodeling, and those in which remodeling was Ͻ0% were considered to have negative remodeling. Percent lipid core and macrophage count at the plaque were assessed.

Quantitative studies on the sinoatrial (SA) node and internodal tracts in IOO heartsfrom patients coming to necropsy with atrialfibrillation have been carried out. In patients with atrialfibrillation developing only in the last two weeks of life, pulmonary emboli and acute pericarditis were common precipitating factors. Atrial dilatation was common but the SA node and internodal tracts were within normal limits. In contrast patients with long-term atrial fibrillation showed combinations of nodal artery stenosis, muscle loss in the SA node or internodal tracts, and atrial dilatation. The pathological conditions found most commonly were chronic rheumatic valve disease, ischaemic heart disease, hypertension, and cor pulmonale. Atrialfibrillation in some aged patients was associated with loss of muscle fibres in the SA node without any clear pathological cause.The sinoatrial (SA) node is now universally accepted as the site of initiation of the impulse for cardiac contraction; it is also well established that specialized myogenic fibres are responsible for its inherent rhythm (HofEman and Cranefield, I960). The impulse passes to the atrioventricular node via internodaltracts within the atria (James, i96i, I963) and, while in man these tracts do not have specific histological features, there is ample physiological proof of their existence (Vassalle et al., I964).Great emphasis has always been placed on the pathophysiological basis of atrial fibrillation, both in man and animals. The morphological changes which may predispose to or accompany this arrhythmia have received considerably less attention. Clinical studies in man have shown conditions such as rheumatic valve disease to be strongly associated with atrial fibrillation (Stock, I970). Old age seems both to predispose to atrial fibrillation (Taran and Szilagyi, I958) and to mitigate against DC conversion (Waris, Kreus, and Salokannel, 197I).Though our knowledge of the pathology of atrial fibrillation is far from complete, valuable work has been carried out by Hudson (I965) who suggested that damage to the SA node was one factor. Other features described in this arrhythmia include damage to internodal pathways (James, i962), atrial dilatation (Laas, i962), and occlusion of the nodal artery Received 28 July 1971.(Lippestad and Marton, I967). It is uncertain, however, whether each of these lesions can cause arrhythmia acting singly, or in combination or, indeed, if they are invariably present in atrial fibrillation. It is also probable that in some transitory episodes of atrial fibrillation, as in digitalis therapy, purely physiological mechanisms are acting without structural damage. Materials and methodsHearts were taken from I00 patients with atrial fibrillation coming to necropsy at St. George's Hospital and The Central Middlesex Hospital, London. These patients represent a consecutive series over a one-year period. All the patients had an electrocardiogram recording atrial fibrillation during the last two weeks of life, and cases were only included when clin...

Genes on five loci on separate chromosomes are responsible for a familial disease in which all or part of the ventricular muscle undergoes thickening with a histological picture of irregular hypertrophy and disorganized arrangement of myocytes (disarray). The three genes identified so far encode for beta heavy chain myosin (chromosome 14), troponin T (chromosome 1) and alpha tropomyosin (chromosome 15). It is postulated that the phenotype within the heart is produced by abnormal myofibril formation and alignment leading to an abnormal cell shape and, thus, disarray. While all the myocytes carry the gene, the regional selectivity of the hypertrophy is unexplained. The phenotypic expression of the disease within affected members of one family, all of whom are heterozygous for the same gene abnormality, is very varied. Asymptomatic carriers are common, and new mutations do not account for most apparently isolated cases. The phenotypic expression of the disease was studied in 75 hearts. The increase in total heart weight ranged from near normal to over 800 g. Ventricular involvement was diffuse and symmetric in 42%. The commonest asymmetric form involved the anteroseptal region (31%) but sporadic cases involved only the posterior or lateral wall. A minority of cases (9.5%) did not show macroscopic wall thickening. Fibrosis is often associated with dysplastic changes in the media of small intramyocardial arteries and may lead to the ventricular wall simulating a dilated cardiomyopathy. A subaortic patch of endocardial thickening on the ventricular septum due to contact with the anterior cusp of the mitral valve was found in a third of cases.(ABSTRACT TRUNCATED AT 250 WORDS)