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OBJECTIVES: Recent studies suggest that alterations in tissue thrombolysis as well as the inward migration of cells may be specific events that contribute to coronary artery narrowing after cardiac transplantation. Plasminogen activators and inhibitors play a central role in governing not only tissue thrombolysis, but also vascular cell migration. The purpose of this study was to examine arterial wall expression of the plasminogen activation system in coronary arteries during graft vascular disease initiation and progression. METHODS: Using in situ hybridization and immunocytochemistry, the expression patterns of uPA and PAI-1 in coronary arteries from cardiac allografts were compared to those of young individuals without disease. RESULTS: Both PAI-1 and uPA were over-expressed early after transplantation and as late as 27 months post grafting. Over-expression of these molecules preceded morphological evidence of graft vascular disease. Of special note was the adventitial expression of uPA and PAI-1 in microvessels and myofibroblasts. In contrast, the expression of uPA and PAI-1 in normal coronary arteries was confined to endothelial cells of the central lumen, as well as low levels of expression in intimal and medial smooth muscle cells. CONCLUSIONS: Despite morphologic similarities between normal and transplant coronary arteries, differences were noted in the vascular expression pattern of uPA and PAI-1. The exact role of these molecules in graft vascular disease requires further study; however, it is intriguing to consider that a local imbalance in the plasminogen system may contribute to arterial wall thrombosis and/or excessive cell migration and the genesis of complex vascular lesions.

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Transforming growth factor-beta (TGF-beta) plays an important role in vascular lesion formation and possibly the renarrowing process ("restenosis") that occurs after balloon angioplasty. Secreted in a latent form by most cells, TFG-beta requires enzymatic conversion before it is biologically active. TGF-beta-inducible gene h3 (beta ig-h3) is a novel molecule that is induced when cells are treated with TGF-beta1. This study examined the expression of beta ig-h3 in normal and diseased human vascular tissue. To determine the expression pattern of beta ig-h3 in human arteries, immunocytochemistry was performed on tissue sections from (1) normal internal mammary arteries, (2) the proximal left anterior descending coronary artery (with minimal intimal thickening) of 15 patients aged 18 to 40 years, (3) primary and restenotic coronary lesions from 7 patients, and (4) fresh directional atherectomy tissue from 11 patients. A polyclonal antibody consistently immunodetected beta ig-h3 protein in endothelial cells of all vascular tissue. In normal coronary arteries of young individuals, beta ig-h3 protein was absent from the intima and media but was found in the subendothelial smooth muscle cells of some arteries with modest intimal thickening. In diseased arteries beta ig-h3 protein was more abundant in the intima than the media. Restenotic coronary lesions tended to show higher levels of immunodetectable beta ig-h3 protein, especially in areas of dense fibrous connective tissue. Beta ig-h3 protein was immunodetected in the cytoplasm of plaque macrophages as well as smooth muscle and endothelial cells. By using in situ hybridization on fresh directional atherectomy specimens, we found beta ig-h3 mRNA to be overexpressed by plaque macrophages and smooth muscle cells. Nondiseased human internal mammary arteries also expressed beta ig-h3 mRNA in endothelial cells but not in the smooth muscle cells of the normal intima and media. These results document the expression of beta ig-h3 in diseased human arterial tissue and support the hypothesis that active TGF-beta plays a role in atherogenesis and restenosis.

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A case of deglutition syncope of 20 years' duration in a patient without cardiac or esophageal disease is presented. The therapeutic efficacy of beta-blockade is documented by symptomatic improvement, repeat esophageal balloon inflation and tilt-table testing. This suggests the Bezold-Jarisch reflex or sympathetic nervous system may be involved in the pathogenesis of deglutition syncope.

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A method is described for computerized, operator-assisted, morphometric measurement of histologically prepared arterial cross sections. The system is composed of an image cytometer equipped with a one power lens and a digitizing camera interfaced with an imaging board residing in a PC computer. Algorithms were developed for automated segmentation of the areas of interest. The method is rapid, objective, accurate and requires minimum operator intervention. It gives reliable and reproducible results in the measurement of all elements of the cross section including circumference, area of the media, circumference of the internal elastic lamina, area of the lumen and percent occlusion of the lumen by the intimal thickening. While manual measurements using computerized planimetric methods give similar results, this method is an order of magnitude faster (1-2 min vs. 10-20 min per cross section) thus facilitating the study of large numbers of specimens. A blinded re-measurement of 284 sections of artery for reproducibility yielded r values of 0.86-0.97.

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OBJECTIVE: To describe the extent and distribution of coronary artery luminal narrowing in a Canadian population (aged 40 years and under) dying suddenly and unexpectedly. METHODS: From a coroner's autopsy population of 350 subjects whose mean age was 28.4 +/- 6.5 years and of whom 250 were male, percentage luminal narrowing was estimated in the four epicardial coronaries. The left main, left anterior descending, left circumflex and right major coronary arteries were sectioned at 5 mm intervals and percentage cross-sectional luminal narrowing from the internal elastic lamina of each segment was estimated microscopically and then graded into four categories: I, 0 to 25%; II, 26 to 50%; III, 51 to 75%; and IV, greater than 75%. A total of 14,611 5 mm segments were evaluated (mean 41.7 per case). The segments were classified as originating from males or females and into three age groups (less than 20, 20 to 29 and 30 to 40 years). RESULTS: For the entire population, virtually no luminal narrowing greater than 50% was found in patients less than age 20 years, but was found in 3% of segments in the group aged 20 to 29 years and in 8.4% of segments in the group aged 30 to 40 years. In the group aged 20 to 29 years, greater than 50% narrowing was found in 3.8% of segments in males and in 1.2% of segments in females (P < 0.001). In the group aged 30 to 40 years, the corresponding numbers were 10.5% for males and 2.2% in females (P < 0.0001). Eighty-six males (34.4%) had greater than 50% narrowing of at least one coronary artery versus 19 females (19%) (P < 0.01). Left main narrowing of greater than 50% was found in 17 subjects, of which 13 were males. Luminal narrowing was more prevalent in the left anterior descending than the right coronary artery or left circumflex coronary artery and more prevalent in the right coronary artery than the left circumflex coronary artery. CONCLUSIONS: In subjects less than age 20 years, luminal narrowing greater than 50% was virtually nonexistent. Its frequency progressed in both sexes after age 20 years and was significantly more pronounced in males. Narrowing of the left main coronary artery was more frequent than anticipated and was more common in males.

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Concern about waiting lists for elective procedures has become a highly visible challenge to the universal health insurance program in Canada. In response to lengthening queues for patients waiting for cardiac surgery, British Columbia made contracts with four Seattle hospitals to send a total of 200 patients for coronary artery bypass surgery. This article examines the cause of the queue for cardiac surgery in British Columbia and the events that led to outside contracting. Global hospital budgets and restrictions on capital expansion have limited hospital capacity for cardiac surgery. This constrained supply, combined with periodic shortages in critical care nurses and cardiac perfusion technologists, has resulted in a rapid increase in the waiting list. Reducing wide variations in the lengths of queues for individual surgeons may afford an opportunity to reduce long waits. While the patient queue for cardiac surgery has sparked a public debate about budget limits and health care needs, its clinical impact remains uncertain.

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Milrinone is a nonglycoside, nonsympathomimetic bipyridine with positive inotropic and systemic vasodilator properties. In order to evaluate the efficacy and safety of a short term infusion of milrinone, 105 patients with stable New York Heart Association (NYHA) class III or IV heart failure received a loading dose (50 micrograms/kg) and a 48 h continuous infusion (0.5 micrograms/kg/min). Administration of the loading dose resulted in a 28% decrease in pulmonary capillary wedge pressure (PCWP) (P less than 0.001), a 38% increase in cardiac index (P less than 0.001), and a 34% increase in stroke volume index (P less than 0.001) within 15 mins. Milrinone infusion maintained an average 27% and 24% reduction in PCWP during the first and second days, respectively (P less than 0.001). Cardiac index was 32% and 34% above baseline during the same intervals (P less than 0.001). There were no clinically significant changes in heart rate or mean arterial blood pressure during the study period. In a subset of 47 patients who underwent Holter monitoring before and during infusion, a significant increase in ventricular arrhythmias (premature ventricular complexes per hour, ventricular couplets per hour and ventricular runs greater than or equal to three) was demonstrated (P less than 0.0001). In general, milrinone was well tolerated. Of the 105 patients entered, one died of an acute myocardial infarction after premature termination of the infusion, and the infusion rate was decreased in two others because of supraventricular arrhythmias. In patients with severe heart failure, intravenous milrinone has significant beneficial hemodynamic effects. ECG monitoring for arrhythmias is recommended during milrinone infusion.

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This study is a prospective report of the cases of 135 patients who were slated for coronary artery bypass grafting and selected according to designated criteria. Patients received, in addition to an interview, a comprehensive cognitive, neuropsychologic, and personality assessment 2 weeks before operation and 3, 12, and 24 months after operation. Of the available sample, 82.3% completed the full study. There was no evidence of intellectual or neuropsychologic impairment after operation. Most patients returned to preoperative status 3 months after bypass grafting. Further improvement may continue 12 and 24 months after operation. The personality tests revealed that anticipation of the operation resulted in signs of emotional arousal and distress, which dissipated after a successful surgical outcome. Similarly, return to work and quality of life was enhanced. The current study represents the first systematic, longer-term follow-up of the psychologic and social consequences of coronary artery bypass grafting operations. The findings of this study are discussed within a model of social reconstitution after the successful resolution of a life-threatening medical condition.

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A patient with resistant ventricular tachycardia treated with a combination of antiarrhythmic agents is described. Sudden onset of a wide complex ventricular rhythm with periods of asystole and failure to achieve transvenous pacing were observed, presumably due to antiarrhythmic drug toxicity. Inability to pace was reversed by the infusion of isoproterenol.

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The calcium channel blockers provide an exciting and effective new therapeutic tool in the management of ischaemic cardiac syndromes and may prove popular and effective in the treatment of a variety of other disorders. They have provided a new approach to treatment and have added new insights into the pathogenesis of ischaemic cardiac syndromes. Their introduction into clinical practice has been swift and many of our concepts regarding their pharmacologic activities in man remain based on theoretic considerations. Their expanding clinical use and further comparative studies will undoubtedly provide further information in regard to indications, adverse effects, drug interaction and long-term safety. Particular caution is advised when they are combined with certain antiarrhythmic agents, digitalis and particularly beta adrenergic blocking agents. Little is known about their interaction with various general anaesthetic agents and for this reason particular vigilance is required as more patients receiving these agents are admitted for surgical procedures.

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A subgroup of 22 patients with variant angina who had responded well to calcium antagonist drugs were studied to determine if ergonovine testing could help assess the need for continued therapy. Before treatment all 22 patients exhibited angina with S-T elevation during ergonovine testing done in the coronary care unit according to a previously described protocol with sequential ergonovine doses of 0.0125, 0.025, 0.05, 0.1, 0.2, 0.3 and 0.4 mg administered at 5 minute intervals. After 9.4 +/- 4.7 (range 1 to 24) months of treatment (nifedipine 7 patients, diltiazem 3, verapamil 8, perhexiline 3, nifedipine and diltiazem 1), all patients were free from anginal attacks. Medication was discontinued and ergonovine testing repeated 24 to 48 hours later (3 weeks for perhexiline). In 12 of the 22 patients, angina or S-T segment shifts did not occur during the second ergonovine test to a maximal dose of 0.4 mg. Treatment was not restarted in these patients and all 12 remain free of variant anginal attacks 4.2 +/- 2.9 (range 1 to 13) months later. In seven patients angina and S-T elevation occurred during the second ergonovine test, in the same electrocardiographic leads as during the test before treatment. In three patients the ergonovine test induced angina with S-T depression in the leads where S-T elevation had occurred during the previous test. Treatment was reinstituted in these 10 patients with a positive test. No complications resulted from ergonovine testing in any patient. We conclude that in many patients with variant angina, symptoms will disappear spontaneously and the ergonovine test will revert to negative. Treatment with calcium antagonist drugs can probably be safely discontinued in some patients with variant angina; ergonovine testing appears to be helpful in identifying such patients. Longer periods of follow-up are required to confirm that symptoms do not recur.

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This study describes the results of ergonovine testing in 100 consecutive patients who underwent this procedure in a coronary care unit. All patients had recently undergone coronary arteriography. A bolus injection of ergonovine was administered at 5 minute intervals in the following doses (mg): 0.0125, 0.025, 0.05, 0.1, 0.2, 0.3 and 0.4. The criterion for a positive test was the appearance of S-T elevation greater than 1 mm. The test was positive in all 17 patients known to have variant angina and in 18 (40 percent) of 45 patients who had a history of chest pain judged strongly suggestive of variant angina but who had no electrocardiogram recorded during pain. Of 38 patients with a history of chest pain classified as not entirely typical of variant angina, only 1 (2.6 percent) had a positive test. Of the 64 patients with a negative ergonovine test, 47 had chest pain and 25 had nausea but none had more serious complications. Ventricular arrhythmia accompanied S-T elevation in 18 of the 36 patients with a positive test but occurred in only 4 of the 64 with a negative test (p < 0.0005). No patient needed treatment with antiarrhythmic drugs. Four of the 36 patients with a positive test had serious complications: severe transient hypotension (2 patients), recurrent episodes of angina with S-T elevation (1 patient) and a subendocardial infarction (1 patient). Thus, ergonovine testing is useful in patients with a typical clinical history of variant angina but without an electrocardiogram recorded during pain. In this study, a small but definite incidence of serious complications occurred during a positive test.

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The hemodynamic effects of a single oral dose of 20 mg of nifedipine were studied in 21 stable patients after an acute myocardial infarction before withdrawal of Swan-Ganz and intra-arterial catheters. The drug appears safe, and no significant untoward effects were noted. Significant hemodynamic changes were present between 15 and 120 minutes after ingestion with a peak at 60 minutes. Mean arterial pressure decreased from 81+/-2.7 (SEM) to 71+/-2.3 mm Hg (P<0.001), and systemic vascular resistances decreased from 1438+/-88 to 1144+/-63 dynes/sec/cm5 (P<0.001). Cardiac index increased from 2.7+/-0.1 to 3.1+/-0.1 L/min/sq m (P<0.01) and heart rate from 79 +/- 3 to 82 +/- 4 (P<0.01). The pressure-rate product decreased from 10.3 X 10(3) to 9.5 X 10(3) (P<0.05), and pulmonary wedge pressure was unchanged from 12 mm Hg. The hemodynamic changes were similar whether patients were receiving propranolol or not. The afterload reducing effect was potentially most beneficial in the subgroup of patients with depressed left ventricular function where cardiac index increased by 20 percent.

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