Life adaptation after percutaneous transluminal coronary angioplasty and coronary artery bypass grafting.

Life adaptation of 32 patients who had undergone percutaneous transluminal coronary angioplasty (PTCA) for coronary stenosis was compared with that of 15 patients who had coronary artery bypass grafting (CABG). Patients were matched for psychosocial, anatomic and cardiac functions. Life adaptation was measured at 6 and 15 months after PTCA or CABG by the Psychosocial Adjustment to Illness Scale (PAIS), a multidimensional instrument that evaluates change in 7 primary life domains. The overall PAIS scores for patients who had undergone PTCA were significantly better (p less than 0.04) than the scores for those who had undergone CABG after 6 months, and this superior functioning continued after 15 months (p less than 0.05). After 6 months patients who had undergone PTCA functioned better at work (p less than 0.005), in sexual performance (p less than 0.0001) and with their families (p less than 0.002). The improvement in work functioning continued at 15 months (p less than 0.04), but the differences in sexual and family domains became nonsignificant.

Exercise-induced ST segment elevation in a patient with effort angina pectoris and normal coronary arteries.

A 32 year old woman who complained of exercise-induced chest pain was found to have widespread elevation of the ST segment of the electrocardiogram during exercise testing. Coronary angiography demonstrated no obstructive lesions and no evidence of coronary artery spasm despite ergonovine administration, bicycle ergometry and rapid atrial pacing. Exercise thallium-201 scintigraphy demonstrated no perfusion defects despite ST segment elevation. Radionuclide blood pool imaging revealed a slight decrease in ejection fraction with exercise. The available evidence raises the possibility of small vessel coronary artery disease, either structural or vasotonic, as a cause of this patient's symptoms.

Inhalation challenge with carbachol and isoproterenol to predict bronchospastic response to propranolol in COPD.

Disabling propranolol-induced bronchospasm occasionally prevents use of this drug in patients with chronic obstructive pulmonary disease (COPD). A means was developed to identify patients who have high risk for this adverse effect using bronchial challenge by inhaling the parasympathomimetic drug, carbachol, and isoproterenol. After baseline pulmonary function tests, 12 patients with varying degrees of COPD and 13 control patients underwent maximal beta-blockade using intravenously administered propranolol during cardiac catheterization followed by repeat pulmonary function testing. Seven of the patients with COPD and ten of the control subjects were restudied while taking propranolol orally for at least three weeks. The results indicated that the bronchodilator response to inhaled isoproterenol does not reliably identify patients who develop bronchoconstriction with propranolol, but bronchoconstriction after inhaling carbachol is indicative of the high risk of developing bronchoconstriction from propranolol.

Multiformity if induced unifocal ventricular premature beats in human subjects: electrocardiographic and angiographic correlations.

Single ventricular premature responses induced by strength-interval pacing were elicited at multiple sites in 30 patients undergoing cardiac catheterization to determine if and under what circumstances unequivocally unifocal stimulated ventricular premature beats could manifest multiformity of the QRS configuration. Multiformity was defined as unifocal responses whose mean frontal axes differed by greater than 15 degrees with or without associated morphologic differences in the horizontal leads. Multiformity occurred in 12 (40 percent) of 30 patients. A statistically significant association was found between multiformity and the presence of a quantitatively defined left ventricle wall motion abnormally (p less than 0.01), prior myocardial infarction (p less than 0.01) and a left ventricular election fraction of less than 0.60 (p less than 0.05). Twelve (67 percent) of the 18 patients without multiformity had coronary artery disease, but only 4 of those 12 had a left ventricular wall motion abnormally or prior myocardial infarction, or both. Multiformity was also dependent on the site of stimulation and on the degree of prematurity. The results of this study indicate that the QRS configuration of early premature beats cannot be relied on as a predictor of their site of origin and multiformity is not necessarily synonymous with multifocality.

Aortic rupture into the esophagus during angiography.

A 67-year-old woman was examined and found to have symptoms and chest roentgenogram suggesting acute aortic dissection. During emergency angiography, massive upper gastrointestinal bleeding developed, and the woman died. The angiogram showed a raised intimal flap of acute dissecting aneurysm. Postmortem examination showed extensive cystic medial necrosis, aortic dilation, and an unusual combination of anatomic abnormalities, which explained the previously unreported false-positive intimal flap. The site of aortic rupture was not localized, but a large tear was found in the esophagus.

Hemodynamic and respiratory effects of morphine and butorphanol.

The hemodynamic effects of butorphanol, a potent synthetic narcotic-antagonist analgesic, were investigated and compared with those of morphine. A total of 20 patients were studied (8 butorphanol, 12 morphine) at the time of diagnostic cardiac catheterization. Butorphanol decreased pH, PCO2, and systemic artery pressure and increased PCO2, cardiac index, and pulmonary artery pressure. Morphine caused similar changes in pH, PO2, systemic artery pressure, and PCO2 but much smaller changes in cardiac index and no change in pulmonary artery pressure. The clinical implications and possible mechanisms are discussed.

Postextrasystolic potentiation as a predictor of potential myocardial viability: preoperative analyses compared with studies after coronary bypass surgery.

The ability to predict reversibility of ventricular dysfunction should be important in determining operability. This study examined the usefulness of postextrasystolic potentiation as such a predictor. Left ventricular wall motion was studied using cineventriculography in 31 patients before and after revascularization surgery. Preoperative ejection fraction and wall motion were analyzed during a sinus beat and after a random ventricular extrasystole, whereas postoperative ejection fraction and wall motion were examined only during a sinus beat. Changes in ventricular motion were correlated with changes in vascular supply achieved by operation. Of the 7 patients whose ejection fraction was improved postoperatively, 6 had shown postextrasystolic potentiation compared with only 10 of the 24 patients without such improvement (P less than 0.05). Regional wall motion analysis also showed a significant association between postextrasystolic potentiation and postoperative improvement in wall motion. Of 26 zones judged to have an increased vascular supply after operation, 11 showed increased motion postoperatively. All 11 had shown postextrasystolic potentiation, compared with only 5 of 15 zones with increased vascular supply but without increased postoperative motion (P less than 0.001). Thus, postextrasystolic potentiation seems to be a useful predictor of the ability of asynergic myocardium to respond to successful revascularization surgery.

Abnormalities of left ventricular function and geometry in adults with an atrial septal defect. Ventriculographic, hemodynamic and echocardiographic studies.

Left ventricular function and motion in 12 adults with an ostium secundum atrial septal defect were analyzed utilizing biplane cineangiography. Values for left ventricular end-diastolic volume index, stroke volume index, ejection fraction, left ventricular end-diastolic pressure and mean rate of circumferential fiber shortening were compared with values in an age-matched group of 11 normal subjects. Comparisons of ventriculographic and echocardiographic data were also made in 5 patients and 10 control subjects. Cardiac index was smaller in patients than in the normal subjects (3.6 vs. 4.5 liters/min per m2, P less than 0.01). Although left ventricular end-diastolic pressure was similar (8 mm Hg in both groups), the end-diastolic volume index was significantly smaller in patients than in normal subjects (56 vs. 76 ml/m2, P less than 0.05). Stroke volume index was also significantly smaller in patients (40 vs. 52 ml/m2, P less than 0.01). The two groups had similar values for ejection fraction (65 +/- 2 percent [standard error of the mean] in patients vs. 68 +/- 2 percent in normal subjects), circumferential fiber shortening velocity (1.67 +/- 0.13 vs. 1.81 +/- 0.15 circumferences/sec.), heart rate (91 +/- 7 vs. 90 +/- 5 beats/min) and mean systemic arterial pressure (92 +/- 5 vs. 87 +/- 3 mm Hg). Early systolic bulging of the upper ventricular septum toward the right ventricle was seen in 10 of 12 patients with an atrial septal defect but in no normal subject. Echocardiographic data supported these findings. No other abnormalities of motion were consistently noted. It is concluded that the left ventricle of patients with an atrial septal defect is subnormal in volume and abnormal in sequence of contraction of the septum and is characterized by apparent decreased distensibility.