[Disease of the small coronary vessels].
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OBJECTIVES: This study evaluated the relation between reversible segmental left ventricular dysfunction and frequency domain measures of heart period variability in patients with coronary artery disease. BACKGROUND: Heart period variability is frequently reduced in patients with coronary artery disease. However, the mechanisms of this reduction are still unclear. METHODS: Echocardiographic left ventricular wall motion and frequency domain measures of heart period variability were evaluated in 32 patients with one-vessel coronary artery disease before and 16 to 24 days after successful percutaneous transluminal coronary angioplasty. Of these, 12 patients (Group A) had normal and 20 patients (Group B) had abnormal regional wall motion. A control group of 15 healthy subjects (Group C) underwent 24-h Holter recording twice at 2-week intervals to check for spontaneous variations. RESULTS: At baseline, low and high frequency power were lower in Group B than in Groups A and C, whereas no difference was detectable in ultra low and very low frequency and total power. After coronary angioplasty, regional wall motion and frequency domain measures of heart period variability were unchanged in Group A. In Group B the mean (+/- SD) summed segment score improved from 17.1 +/- 3.6 to 12.8 +/- 2.0 (p < 0.01), and mean low and high frequency power (logarithmic units) increased from 6.14 +/- 0.23 to 6.35 +/- 0.34 (p < 0.01) and from 5.43 +/- 0.32 to 5.68 +/- 0.52 (p < 0.01), respectively. Furthermore, low and high frequency power, lower at baseline in Group B than in the other two groups, were comparable in the three groups after coronary angioplasty. CONCLUSIONS: This study demonstrates that segmental left ventricular dysfunction is involved in determining sympathovagal imbalance in patients with one-vessel coronary artery disease; the reversal of left ventricular dysfunction by successful coronary angioplasty improves the heart period power spectrum. Thus, alterations in cardiac geometry influence the discharge of afferent sympathetic mechanoreceptors, contributing to the derangement in autonomic control of heart rate.
The effect of saponin and blockade of the nitrogen oxide upon the coronary endothelium was found in rats subjected to a 6-hrs stress. The damage of the endothelium and the blockade abolished the stressor-induced increase in the coronary blood flow velocity. The index of autoregulation and the latter's efficiency, however, remained the same. Preliminary administration of L-arginine prevented the effect of NG-monomethyl-L-arginine upon the coronary flow in the isolated hearts of rats subjected to stress. The post-stressor increase in the coronary blood flow seems to be due to an increase in releasing the nitrogen oxide from the coronary vessels' endotheliocytes.
The direct effects of extrinsic nerve stimulation on coronary artery tone are unclear because of the complications arising from alterations in myocardial dynamics which themselves alter flow. An isolated and perfused nonbeating slab of beef ventricle was utilized in the present experiments to eliminate secondary complications and the efects of periarterial nerve activation on coronary perfusion pressure were examined. It was found that stimulation induced vasoconstrictor responses which were enhanced by physostigmine, a cholinesterase inhibitor, and blocked by atropine. These responses were duplicated by exogenous acetylcholine both in the perfused preparation and in isolated strips of coronary artery. Although added noradrenaline gave vasodilatation, no response attributable to the release of noradrenaline from nerves was obtained. It is concluded that the coronary vasculature of the beef receives a cholinergic innervation and that its activation, especially under conditions of reduced transmitter degradation, may induce considerable coronary vessel constriction.
In 22 patients with single-vessel coronary artery disease and no history of infarction, stress Tl-201 rotational tomography was used to quantify the extent of jeopardized myocardium. The vertical long- and short-axis tomograms were quantified by means of maximum-count circumferential profile analysis. The scintigraphic extent of jeopardized myocardium was expressed as the percentage of profile points falling 2.5 standard deviations below a previously established mean normal profile and was correlated to a quantitatively expressed angiographic extent of jeopardized myocardium. The extent of jeopardized myocardium varied from 1% to 55% by tomography and 8% to 50% by angiography and correlated with an r = 0.79 and a 10% standard error of the estimate. Defect intensity, reflecting the mean depth by which the abnormal points fell below the normal value of greater than or equal to 10%, was 100% specific for a coronary stenosis of greater than or equal to 70%. In conclusion, this study demonstrates that: patients with single-vessel disease have highly variable extents of hypoperfused myocardium defined by Tl-201 tomography and coronary arteriography, there is a fair relationship between angiographic jeopardy score and perfusion defects by Tl-201 tomography during exercise, and Tl-201 tomography may be used to noninvasively determine the extent of hypoperfused myocardium in coronary artery disease.
We studied six patients who suffered from angina pectoris but had angiographically patent major coronary arteries. Two of the patients suffered also from congestive heart failure. Three patients had supraventricular tachyarrhythmias. Three patients had conduction disturbances. During coronary angiography the patients had significantly reduced flow velocity of angiographic contrast medium compared with that in a control group. Echocardiographic and Doppler flow studies showed a tendency for symmetrical thickening of the left ventricular wall, enlargement of the right ventricle, and reduced compliance of both ventricles. Right ventricular endomyocardial biopsy revealed pathologic small coronary arteries with fibromuscular hyperplasia, hypertrophy of the media, myointimal proliferation, and endothelial degeneration. Capillaries had swollen endothelial cells encroaching on the lumen. Myocardial hypertrophy, lipofuscin deposition, and patchy fibrosis were also observed. These cases show that small-vessel coronary artery disease can cause classic angina pectoris. The diagnosis can be suspected when the coronary angiogram shows large patent arteries with slow flow of the angiographic contrast medium and it can be confirmed by endomyocardial biopsy.
BACKGROUND: The value of off-pump in situ left internal thoracic artery to left anterior descending coronary artery bypass grafting in single-vessel coronary artery disease was assessed by long-term angiographic and clinical data. METHODS: One-hundred three randomly selected patients (87 male, 16 female; mean age, 57.4 +/- 10.5 years) underwent postoperative angiographic control after an average postoperative period of 4.8 +/- 2.9 years (up to 8.2 years; a total of 490 patient-years). RESULTS: Fifty-five patients (52%) were asymptomatic, whereas 31 (30%) had anginalike chest pain. Ninety-seven patients (94.2%) were in New York Heart Association class I or II. Five-year angina-free survival was 81% +/- 5%. Of 103 left internal thoracic arteries assessed, 99 were patent (overall patency, 96.1%). All four cases having occluded grafts had mild native vessel stenoses (<80%) before operation. The patency rate was 99% +/- 1% at 3 years, and 93% +/- 4% at 5 years. The left ventricular segmental wall motion score of the left anterior descending coronary arterial distribution improved from 4.1 +/- 1.1 to 3.7 +/- 0.9 (p = 0.001). Consequently, 15 patients (15%) underwent secondary revascularization (11 interventional and 4 surgical) 4.8 +/- 2.1 years after the primary operation. The most frequent indication for interventional revascularization was atherosclerotic progression in systems other than left anterior descending artery. The cases with graft occlusion were treated surgically. Five-year freedom from interventional or surgical repeat revascularization was 91% +/- 4%. CONCLUSIONS: In addition to the well-documented safety and reliability, off-pump in situ left internal thoracic artery grafting is also a durable treatment for isolated left anterior descending artery disease, in both clinical and angiographic terms.
BACKGROUND: Patients with multi-vessel coronary artery disease (CAD) are selected for percutaneous coronary interventions (PCI) or surgical revascularisation. The appropriateness of "ad hoc" PCI of borderline lesions (<70% of lumen diameter) in patients with a multi-vessel CAD has not been proven. However, delayed PCI of another lesion and gaining additional information from non-invasive tests is not a widely accepted strategy. When left anterior descending (LAD) coronary artery is one of the affected vessels, selection for surgical revascularisation is most likely. AIM: To assess long-term outcome in patients with multi-vessel CAD and borderline lesions, including LAD, in whom fractional flow reserve (FFR) in all affected vessels was measured and used for selection for PCI or conservative treatment. METHODS: The study group consisted of 16 patients with stable angina (11 males, mean age 60+/-9 years) with 34 lesions localised in the main epicardial coronary arteries [LAD / left main (LM) / right coronary artery (RCA) / intermediate branch (IB) / circumflex artery (Cx) - 15/1/5/5/8] of which at least two were borderline stenoses. Each lesion underwent FFR measurement. "Ad hoc" PCI was performed when FFR was <0.75, and conservative therapy was instituted when FFR was >0.75. RESULTS: Of 34 lesions, in 8 (23%) the FFR value was <0.75 and these lesions were treated with PCI (LAD/IB/Cx - 3/2/3). In the remaining 26 (77%) lesions, FFR was >0.75 and conservative therapy was instituted. During the mean follow-up of 15+/-6 months (range 6-28 months, median 15 months) in 8 of 9 conservatively treated patients no aggravation of anginal symptoms nor other coronary events were observed. One patient developed acute myocardial infarction due to thrombus occluding a borderline LAD lesion. Of 8 lesions treated with PCI (baseline FFR = 0.63+/-0.10 vs post-PCI FFR = 0.92+/-0.08, p=0.0002), in one case an in-stent restenosis in LAD occurred 9 months after PCI. Of a total of 26 lesions which were conservatively treated (mean FFR 0.91+/-0.05), in 2 (7.7%) the progression of CAD was noted. CONCLUSIONS: In patients with multi-vessel CAD and borderline lesions, FFR measurement identifies those, who can be treated conservatively with a good long-term outcome, and prevents unnecessary PCI.
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The optimal treatment of patients with single-vessel coronary artery disease (CAD) and chronic stable angina is controversial. Therapeutic options include medical therapy with pharmacologic agents and/or coronary revascularization via surgery (coronary artery bypass grafting [CABG]), percutaneous transluminal coronary angioplasty (PTCA), and/or other transcatheter techniques. Early studies found no difference in survival between medical and surgical treatment of patients with single-vessel disease and chronic stable angina. Although PTCA has been shown to improve symptoms and quality of life in patients with single-vessel disease and severe symptoms, improvement in survival and prevention of future events are not established and multiple PTCA procedures or subsequent surgical treatment may be necessary. Medical therapy may be preferred in patients with mild or no symptoms. In patients with chronic stable angina, PTCA practice may not be consistent with current guidelines, particularly obtaining laboratory evidence of ischemia before the procedure. Stenoses that may lead to future coronary events cannot be accurately identified by angiography without evidence of ischemia or symptoms. Currently available comparative studies of patients with CAD do not reflect the impact of stent procedures and aggressive lipid lowering. Therefore, diagnostic and treatment options should be individualized in patients with single-vessel disease and chronic stable angina, and additional randomized trials are necessary to determine the optimal management of these patients.
We examined our practice of invasive therapy for one- and two-vessel coronary disease to assess the impact of the randomized trials of coronary surgery and the current use of angioplasty. We first reviewed our results with coronary artery bypass graft in equivalent patients in the Coronary Artery Surgery Study with one- and two-vessel disease between 1976 and 1981. Among 1376 patients, hospital mortality was 0.07%, and 5-year survival was 95.2% +/- 0.8%. To define trends in invasive therapy, which have since occurred, we compared 100 patients with one- and two-vessel disease in each of three groups: 1979 coronary artery bypass graft, 1984 coronary artery bypass graft, and 1984 percutaneous transluminal coronary angioplasty. Preoperative characteristics in the average 1979 and 1984 patients were similar; however, in 1984, patients who had a coronary artery bypass graft were older than patients who had percutaneous transluminal coronary angioplasty (61.5 versus 56.7 years, p less than 0.01), they required more heart medications (2.1 versus 1.5, p less than 0.01), had more previous infarctions (0.8 versus 0.5, p less than 0.01), and more patients had an ejection fraction of less than 50% (34% versus 7%, p less than 0.01). Patients who had angioplasty had a shorter postoperative stay (median number of days 7, 7, 2, p less than 0.01). Freedom from major complications was similar among the groups (91%, 87%, 85%). Unstable symptoms were the most frequent indication for invasive therapy (approximately 80%), whereas long-term symptoms, those considered in the randomized trials, occurred in relatively few patients. The number of patients without at least one definite indication for invasive therapy was 13%, 3%, and 11%, p less than 0.05, suggesting that the indications for the 1984 coronary artery bypass graft group have become more restrictive since the 1979 coronary artery bypass graft group. Indications for the 1984 percutaneous transluminal coronary angioplasty group remained less restrictive, being similar to those for the 1979 coronary artery bypass graft group. A continuing trend toward the use of percutaneous transluminal coronary angioplasty was evident, as 56% of the 1979 coronary artery bypass graft group of patients and 32% of the 1984 coronary bypass group of patients would be offered percutaneous transluminal coronary angioplasty rather than coronary artery bypass graft on the basis of 1986 percutaneous transluminal coronary angioplasty criteria. The p values were obtained with analysis of variance or chi 2 test.
A patient with a history of Hodgkin's lymphoma presented with recurrent left pleural effusions and dyspnea on exertion 27 years after radiation therapy. Further evaluation disclosed suspected radiation-induced constrictive pericarditis, aortic stenosis and regurgitation, and severe coronary artery disease. He underwent successful 3-vessel coronary artery bypass grafting, aortic valve replacement, and pericardiectomy.
We examined survival rates during a 6-year follow-up of patients in the registry of the Coronary Artery Surgery Study who had three vessel coronary artery disease and Canadian Cardiovascular Society class III-IV angina pectoris. All patients had a stenosis of 70% or greater in either the mid or proximal segment of all three coronary arteries. There were 679 medically treated patients and 1921 surgically treated patients in this nonrandomized comparison. Patients were stratified by left ventricular wall motion score and number of proximal coronary artery stenoses; after adjustment for these variables, the estimated probability of being alive at 6 years was 82% for surgically treated patients and 59% for medically treated patients (p less than 0.0001). Among patients with the most severe left ventricular dysfunction (left ventricular wall motion score of 16 to 30), the 6-year survival rate was 63% for surgically treated patients and 30% for medically treated patients (p less than 0.0001). Those with three proximal lesions (all gradations of left ventricular score) had an 81% 6-year survival rate with surgical treatment and 40% with medical treatment (p less than 0.0001). Ninety percent of surgically treated patients with normal ventricular function were living at 6 years and 78% of medically treated patients (p less than 0.0001). Among these patients, the survival rate was significantly better after surgical treatment than after only medical treatment if two or three proximal stenoses were present. If no proximal lesions were present (all categories of left ventricular function), 84% of surgically treated patients and 67% of medically treated patients were alive at 6 years (p less than 0.0001). In a multivariate (Cox) analysis of preoperative clinical, hemodynamic, and angiographic factors, early operation was a strong predictor of survival (estimated relative risk 0.38).