The dismal outlook for patients with pulmonary atresia with intact ventricular septum may be related to associated right ventricular hypoplasia. Study of 32 autopsy specimens and 46 angiocardiograms of neonates with this lesion suggested that the cavitary hypoplasia was related to massive hypertrophy of the right ventricular wall. This hypertrophy was sufficient to obliterate the trabecular and/or infundibular portion of the ventricular cavity entirely in one-third of the cases; this observation forms the basis for a revised classification of these hearts. Three autopsies and 14 angiograms of neonates with critical pulmonary stenosis were examined. Hearts with obliterated infundibular and trabecular cavities had thicker walls and smaller tricuspid valves, as estimated angiographically or at autopsy, than those in which the normal three portions of the ventricular cavity were represented.

Preoperative, intraoperative and postoperative variables, which might play a role in the development of ventricular conduction defects (VCD) and atrial fibrillation (AF) following coronary artery bypass grafting (CABG), were evaluated in 236 consecutive patients. VCD and AF developed postoperatively in 15.5% of patients: 4.5% had VCD (subgroup A), 11.0% had AF (subgroup B). In 84.5% of patients VCD and AF did not occur (subgroup C). Univariate analysis showed statistically significant differences between subgroups A and C with respect to: left main significant stenoses and number of diseased vessels. Bypass pump time and aortic cross-clamp time were significantly longer in subgroup B. Multivariate analysis showed a significantly greater incidence of left main disease and of right coronary artery occlusion associated with significant stenosis of the proximal left anterior descending artery in subgroup A. In subgroup B, the duration of aortic cross-clamp time was significantly higher. Ischaemic injury, with increasing duration of cardioplegic arrest, seems to play a key role in the development of AF. Nonhomogeneous cardioplegic delivery to critical areas of myocardium, and particularly to the specialized conducting system, may cause VCD after CABG.

Myocardial infarction may cause papillary muscle dysfunction when the blood supply is provided by one rather than two vessels, as is more frequently the case with the posterior rather than the anterior papillary muscle.

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