Endothelial dysfunction in the absence of coronary atheroma causing Prinzmetal's angina.
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Angina Pectoris, Variant↗
Biomedical subjects
J C Kaski
Publications and source records attributed to J C Kaski.
Myocardial beta-adrenoceptor density and plasma catecholamines in syndrome X.
Recent research has cast doubt on the ischemic hypothesis of etiology of syndrome X (anginal pain, ischemic-like changes in the stress electrocardiogram, but normal coronary arteriogram). Abnormalities of pain perception have been shown and abnormal sympathetic nervous system activation has also been implicated. The aim of this study was to test the hypothesis that downregulation of myocardial beta adrenoceptors is demonstrable in patients with syndrome X. Such downregulation would be consistent with raised myocardial catecholamine concentrations. We performed positron emission tomography with (11)C-CGP-12177 to measure beta-adrenoceptor density. Plasma catecholamines were sampled simultaneously and assayed using high-performance liquid chromatography. Twenty syndrome X patients (11 female, age 57 +/- 9 SD years, range 33 to 69) and 18 matched controls (9 women, age 50 +/- 13 years, range 25 to 65; p = NS vs patients) were studied. Myocardial beta-adrenoceptor density did not differ between syndrome X patients and controls: 8.0 (1.9) pmol/g for patients versus 8.3 (2.1) pmol/g for controls; p = 0.62. No differences were found between patients and controls for plasma norepinephrine (2.82 [1.07] and 2.76 [1.18] nM, respectively; p = 0.89) or for epinephrine (0.29 [0.14] and 0.30 [0.20] nM, respectively; p = 0.84). In patients with syndrome X, beta-adrenoceptor density is normal and, by inference, myocardial catecholamines would also be normal. This weakens the case for a generalized enhancement of sympathetic activation in this disorder, although increased sympathetic reactivity during actual episodes of chest pain remains a possibility.
Adrenergic beta-Antagonists↗
Transient autonomic dysfunction precedes ST-segment depression in patients with syndrome X.
Increased sympathetic drive has been suggested to play a role in the pathogenesis of syndrome X (angina pectoris, positive exercise testing, and angiographically normal coronary arteries). Heart rate variability (HRV) studies have shown that patients with syndrome X have an imbalance in autonomic nervous system activity (sympathetic predominance). However, it is not known if transient ST-segment depression which occurs in syndrome X during daily activities is related to this autonomic nervous system dysfunction. This study investigates the relation between the response of the autonomic nervous system, as assessed by HRV analysis, and the occurrence of transient ST-segment depression during 24-hour ambulatory electrocardiographic monitoring in 23 patients (4 men and 19 women, mean age 55 +/- 6 years) with syndrome X. The frequency-domain variables of HRV low-frequency (0.04 to 0.15 Hz) and high-frequency (0.15 to 0.40 Hz) power were measured at 6-minute intervals during the 30 minutes preceding the onset of transient ST-segment depression. Fourteen patients (61%) had > or = 1 episode of ST-segment depression in the 24 hours, whereas the remaining 9 patients (39%) had no significant ST-segment change. HRV measures differed according to whether or not ST-segment depression was associated with increased heart rate. Episodes of ST-segment depression associated with increased heart rate were preceded by a reduction of high-frequency power and an increase in the low-frequency--high-frequency ratio, whereas episodes of ST-segment depression not associated with increased heart rate showed no significant HRV changes. Low-frequency power remained unchanged irrespective of heart rate. Thus, in patients with syndrome X, a sympathovagal imbalance (sympathetic predominance due to vagal tone withdrawal) precedes episodes of ST-segment depression that are associated with an increased heart rate.
Autonomic Nervous System↗
Angiotensin-converting enzyme insertion/deletion polymorphism in angina pectoris with normal coronary arteriograms.
We investigated the relation between angiotensin-converting enzyme gene insertion/deletion polymorphism and syndrome X (angina with normal coronary arteriogram). The results of our study suggest that this polymorphism does not play a major role in the pathogenesis of microvascular angina.
Coronary Angiography↗
Plasma immunoreactive endothelin concentration correlates with severity of coronary artery disease in patients with stable angina pectoris and normal ventricular function.
OBJECTIVES: The present study tested the hypothesis that plasma immunoreactive endothelin concentration correlates with the severity and extent of coronary atherosclerosis. BACKGROUND: Plasma endothelin-1 concentration is increased in patients with unstable coronary syndromes and advanced atherosclerosis. This finding, together with other clinicopathologic observations, suggests that endothelins may participate in the atherogenic process. However, the relation between plasma immunoreactive endothelin and coronary artery disease in patients with stable angina pectoris remains controversial. METHODS: Ninety consecutive patients undergoing coronary angiography for the investigation of exertional chest pain and 49 normal control subjects were prospectively studied. Eleven patients had normal coronary angiographic findings (group I), 65 had coronary artery stenoses (group II), and 14 had coronary artery disease plus symptoms indicating atheroma in other vascular territories (group III). Computerized angiography was used to determine the extent, severity and morphology of coronary stenoses. Plasma immunoreactive endothelin was measured by radioimmunoassay. RESULTS: Mean (+/- SD) plasma endothelin concentration (pg/ml) was significantly higher in patients than in control subjects (7.29 +/- 4.07 vs. 3.48 +/- 1.29, p < 0.0001). Endothelin levels were higher in patients of group III than in those of groups II and I (9.43 +/- 5.48, 7.20 +/- 3.72 and 4.94 +/- 2.89, respectively, p = 0.02). In patients of group II, plasma endothelin correlated with the maximal degree of stenosis in each patient (r = 0.25, p = 0.04) and with the number of stenoses with > or = 70% diameter narrowing (r = 0.36, p = 0.002). The highest plasma endothelin levels were found in patients with total occlusions (8.65 +/- 3.78 vs. 6.46 +/- 3.51 p = 0.02). CONCLUSIONS: Plasma immunoreactive endothelin concentration is increased in patients with chronic stable angina. The higher levels occur in patients with severe stenoses and total coronary occlusion.
Adult↗
Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris.
OBJECTIVES: This study sought to compare the evolution of complex culprit stenoses in patients with stable and those with unstable angina pectoris. BACKGROUND: Complex coronary stenoses are associated with adverse clinical and angiographic outcomes. However, it is not known whether the evolution of complex stenoses differs in unstable angina versus stable angina pectoris. METHODS: We prospectively assessed stenosis progression in 95 patients with unstable angina whose angina stabilized with medical therapy (Group 1) and 200 patients presenting with stable angina (Group 2). After diagnostic angiography, all patients were placed on a waiting list for coronary angioplasty and restudied at 8 +/- 4 (mean +/- SD) months later. In each patient the presumed culprit stenosis was identified and classified as complex (irregular borders, overhanging edges or thrombus) or smooth (absence of complex features). Stenosis progression, as assessed by computerized angiography, was defined as > or = 20% diameter reduction or new total occlusion. RESULTS: At the first angiogram, 364 stenoses > or = 50% and 383 stenoses < 50% were identified. At restudy, 36 (15%) of 236 stenoses progressed in 29 Group 1 patients and 36 (7%) of 502 stenoses in 31 Group 2 patients (p = 0.001). Forty-five (88%) of 51 stenoses > or = 50% and 6 (29%) of 21 stenoses < 50% that progressed developed to total coronary occlusion (p = 0.001). More culprit stenoses progressed in Group 1 than in Group 2 (p = 0.006), whereas progression of nonculprit stenoses was not significantly different in both groups. Culprit complex stenoses progressed more frequently in Group 1 than in Group 2 (p = 0.01). During follow-up, 3 patients died (myocardial infarction), and 51 had a nonfatal coronary event. Culprit stenoses progressed in 15 (54%) of the 28 patients with a nonfatal coronary event in Group 1 and in 9 (39%) of 23 patients in Group 2 (p = NS). Complex morphology (p < 0.001) and unstable angina at initial presentation (p < 0.01) were predictive factors for progression of culprit stenoses. CONCLUSIONS: A larger proportion of culprit complex stenoses progress in unstable angina than stable angina, and this is frequently associated with recurrence of coronary events.
Adult↗
The natural history of unheralded complex coronary plaques.
OBJECTIVES: This study sought to assess the behavior of unheralded complex lesions in patients with no previous history of acute coronary ischemia. BACKGROUND: Angiographically complex coronary stenoses appear to originate from plaque disruption and are associated with rapid progression early and late after acute coronary events. Complex lesions may occur without symptoms, but neither the incidence nor the behavior of these unheralded complex lesions is known. METHODS: We studied 222 patients with chronic stable angina who were on a waiting list for single-vessel percutaneous transluminal coronary angioplasty of an unoccluded lesion and underwent repeat angiography immediately before the procedure as part of routine practice or shortly after a coronary event. Patients with a previous episode of myocardial infarction or unstable angina were not included. Angiograms were analyzed quantitatively and qualitatively using established methods. A change of +/- 15% stenosis severity or total coronary occlusion defined categoric change. RESULTS: At first angiography, there were 52 unheralded complex target lesions (23%) and 170 smooth target stenoses (77%). Stenosis severity did not differ between complex and smooth target lesions at first and second angiography at a mean (+/- SD) interval of 7 +/- 4 months. At follow-up, seven complex lesions had progressed (14%) compared with six smooth lesions (4%, p < 0.02). Total occlusion developed in four complex lesions and one smooth lesion. Overall, complex stenoses progressed by 3 +/- 13% compared with 0.5 +/- 7% in the smooth stenoses (p = 0.15). Complex stenoses were 4.2 times more likely to progress than smooth stenoses (95% confidence interval 1.2 to 15.2 [Cornfields method]). Clinical events developed in seven patients. One complex lesion regressed and became smooth, and three smooth stenoses became complex at follow-up. CONCLUSIONS: Morphologically complex stenosis can develop without an episode of acute coronary ischemia and are relatively common in patients awaiting single-vessel angioplasty. Our study demonstrates that like their clinically heralded counterparts, these unheralded complex stenoses are at higher risk of progression than smooth stenoses.
Angina Pectoris↗
Cardiac imaging in syndrome X: the problem of "reverse redistribution'.
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Coronary Circulation↗
Coronary stenosis progression differs in patients with stable angina pectoris with and without a previous history of unstable angina.
OBJECTIVES: To compare the evolution of stenoses responsible for acute coronary events with those not associated with acute coronary syndromes. METHODS AND RESULTS: We prospectively studied angiographic stenosis progression in 190 stable angina patients, with single vessel disease, who were awaiting non-urgent coronary angioplasty. Sixty four patients had a previous history of unstable angina (Group 1) and 126 patients had no history of unstable angina (Group 2). Culprit stenoses were classified as "complex' or "smooth'. At restudy, 8 +/- 4 months after the first angiogram, 12 of 63 culprit stenoses in Group 1 had progressed and seven of 125 in Group 2 (19% vs 6%, P = 0.0044). Thirteen of 68 complex culprit stenoses had progressed, compared with only 6 of 120 smooth culprit stenoses (19% vs 5%, P = 0.003). Coronary events occurred in 12 Group 1 patients and nine Group 2 patients (P = 0.02). CONCLUSIONS: In patients with stable angina, stenoses associated with previous episodes of unstable angina are more likely to progress than stenoses not associated with previous unstable angina. Unstable coronary atherosclerotic plaques, even those that have been clinically stable for more than 3 months, may retain the potential for rapid progression to total occlusion.
Adult↗
Chest pain during daily life in patients with hypertrophic cardiomyopathy: an ambulatory electrocardiographic study.
Patients with hypertrophic cardiomyopathy frequently complain of chest pain during daily activities. ST-segment depression is described in association with sudden death and pacing, but its prevalence during ambulatory electrocardiographic monitoring is unknown. The aim of this study was to determine the relation of ambulatory ST-segment depression to clinical characteristics, risk factors for sudden death and thallium-201 perfusion in patients with hypertrophic cardiomyopathy. Continuous 48 h ambulatory electrocardiographic monitoring was performed in 113 patients (age 38 +/- 14 years) with hypertrophic cardiomyopathy. Ninety-four (83%) recordings were suitable for ST-segment analysis. A total of 109 episodes of ST-segment depression (> or = 1 mm from baseline) were recorded in 25 (27%) patients (mean 4 +/- 5). In patients < or = 30 years of age (but not > 30) there was an association between ST-segment depression and a history of exertional chest pain (seven of 12 vs one of 20; P = 0.001), and dyspnoea NYHA class II/III (seven of 15 vs one of 17; P = 0.008). There was no association between ST-segment depression and risk markers for sudden death, i.e. family history of sudden death, syncope and non-sustained ventricular tachycardia, in any group. Reversible thallium-201 defects occurred in 27 (29%) of the 94 patients with analysed recordings but were not associated with symptoms, risk factors for sudden death or ambulatory ST-segment depression. In young patients with hypertrophic cardiomyopathy, ischaemia-like ST-segment depression is common and is associated with a history of typical angina and dyspnoea. Reversible thallium-201 perfusion defects are associated with neither symptomatic status nor ambulatory ST-segment depression.
Activities of Daily Living↗
Failure to demonstrate myocardial ischaemia in patients with angina and normal coronary arteries. Evaluation by continuous coronary sinus pH monitoring and lactate metabolism.
BACKGROUND: Whether myocardial ischaemia is the mechanism underlying chest pain in patients with angina and normal coronary arteriograms is controversial. We sought to detect the presence of transient myocardial ischaemia using continuous monitoring of coronary sinus blood pH during atrial pacing. METHODS AND RESULTS: We studied 14 patients (eight women, six men, mean age 51 +/- 3 years) with typical exertional angina and normal coronary arteriograms and nine patients with coronary artery disease (two men, seven women, mean age 61 +/- 7 years). Of the 14 patients with normal coronary arteries, eight had a reduced coronary blood flow reserve (< 2.5-fold increase), 11 had an ischaemic-appearing response to exercise testing, six had reversible perfusion detects on exercise thallium scans and one had resting left bundle branch block. All patients underwent continuous pH monitoring of coronary sinus blood at rest and during incremental atrial pacing (up to 160 bpm). Coronary sinus oxygen saturation and myocardial lactate extraction ratio were also evaluated at rest and at peak pacing. Eleven patients with angina and normal coronary arteries and eight with coronary artery disease had angina during pacing. Both patients with angina and normal coronary arteries (n = 13) and patients with coronary artery disease (n = 9) showed a fall in coronary sinus pH (-0.02 +/- 0.02 vs -0.11 +/- 0.03 pH units, respectively, P < 0.01). Coronary sinus oxygen saturation expressed as a percentage dropped by 19 +/- 6% in patients with coronary artery disease and by 6 +/- 2% in patients with angina and normal coronary arteriograms (P < 0.05). Myocardial lactate extraction ratio decreased from 33 +/- 6% to -1.4 +/- 4% in patients with coronary artery disease and from 23 +/- 8% to 20 +/- 8% in those with angina and normal coronary arteriograms. Three patients with angina and normal coronary arteries had a drop in coronary sinus pH > 0.02 pH units (-0.043 +/- 0.006 pH units) and in coronary sinus oxygen saturation > 8% (16 +/- 3%) consistent with myocardial ischaemia. CONCLUSION: Despite severe chest pain and reduced coronary flow reserve after pacing, most patients with angina and normal coronary arteriograms do not show metabolic evidence of myocardial ischaemia.
Adult↗
Changes in coronary sinus pH during dipyridamole stress in patients with hypertrophic cardiomyopathy.
OBJECTIVES: The presence of angina pectoris and myocardial scarring in patients with hypertrophic cardiomyopathy (HCM) suggests that myocardial ischemia is a factor in the pathophysiology of the disease. The clinical evaluation of ischaemia is problematic in HCM as baseline electrocardiographic abnormalities are frequent and thallium-201 perfusion abnormalities correlate poorly with anginal symptoms. Coronary sinus pH measurement using a catheter mounted pH electrode is a validated sensitive technique for the detection of myocardial ischaemia. METHODS AND RESULTS: 11 patients with HCM and chest pain (eight men; mean (SD) (range) age 36 (11) (19-53) years) and six controls (two men; mean (SD) (range) age 49 (11) (31-62) years) with atypical pain and normal coronary angiograms were studied. Eight patients with HCM had baseline ST segment depression of > or = 1 mm and four had reversible perfusion defects during stress 201TI scintigraphy. A catheter mounted hydrogen ion sensitive electrode was introduced into the coronary sinus and pH monitored continuously during dipyridamole infusion (0.56 mg/kg over four min). The maximal change in coronary sinus pH during dipyridamole stress was greater in patients with HCM than in controls (0.082 (0.083) (0 to -0.275) v 0.005 (0.006) (0 to -0.012), P = 0.02). In six patients (four men; mean (SD) (range) age 29 (9) (19-40 years) the development of chest pain was associated with a gradual decline in coronary sinus pH (mean 0.123 (0.089)), peaking at 442 (106) s. There were no relations among left ventricular dimensions, maximal wall thickness, and maximum pH change. In patients with HCM there was a correlation between maximum pH change and maximum heart rate during dipyridamole infusion (r = 0.70, P = 0.02). CONCLUSION: This study provides further evidence that chest pain in patients with HCM is caused by myocardial ischaemia. The role of myocardial ischaemia in the pathophysiology of the disease remains to be determined but coronary sinus pH monitoring provides a method for quantifying and prospectively assessing its effects on clinical presentation and prognosis.
Adult↗
Low-dose cyclosporine treatment fails to prevent coronary luminal narrowing after heart transplantation.
BACKGROUND: Cyclosporine has been reported to induce endothelial dysfunction, arterial vasculitis, and accelerated atherosclerosis in experimental models. The purpose of the present study was to evaluate whether low-dose cyclosporine treatment started 1 year after heart transplantation reduces graft coronary artery narrowing compared with conventional cyclosporine doses. METHODS: One year after heart transplantation, 30 patients were randomly assigned to receive low-dose cyclosporine A (whole-blood polyclonal cyclosporine target trough levels 200 to 400 micrograms/L; group A; n = 15) or usual cyclosporine dosage (target levels 400 to 600 micrograms/L; group B; n = 15). Proximal and distal diameters of the left anterior descending, circumflex, and right coronary arteries were measured by quantitative coronary angiography at baseline (1 year after transplantation) and at 2 and 3 years after transplantation. RESULTS: One major cardiac event occurred in group A (retransplantation) and two in group B (sudden deaths). Moderate to severe allograft rejection (International Society for Heart and Lung Transplantation score 3A or higher) occurred in seven patients in group A and five in group B during the study period. Mean biopsy sample rejection score during the same period was increased in group A compared with that in group B (1.44 +/- 0.63 versus 1.05 +/- 0.59; p < 0.05). New angiographic evidence of vascular disease was observed in four patients of group A and in one patient of group B. Proximal coronary artery diameter was slightly, although not significantly, reduced in both groups at follow-up angiography. Distal segments showed a significant diameter reduction, which was greater in group A than in group B (-9.7% +/- 1.1% and -5.2% +/- 1.3%, respectively; p < 0.05). CONCLUSIONS: Cyclosporine dose reduction started 1 year after heart transplantation is ineffective in reducing coronary luminal narrowing and may be associated with an increased prevalence of cardiac allograft vasculopathy, especially in the distal coronary tree. Low-dose cyclosporine treatment may slightly enhance the risk of allograft rejection. Further investigations are needed to evaluate the effects of cyclosporine dose reduction started at an earlier time after heart transplantation.
Adult↗
Factor V Leiden polymorphism (FV Q506) in patients with ischaemic heart disease, and in different populations groups.
A point mutation in the factor V gene (FV Q506) renders factor V resistant to inactivation by activated protein C. The frequency of this mutation is known to be significantly increased in patients with thrombophilia. There are conflicting reports on the significance of the polymorphism in patients with ischaemic heart disease. We determined the frequency of FV Q506 in a control Caucasian population, and compared it with 192 Caucasian patients admitted to coronary care and assessed as having myocardial infarction (MI) or unstable angina plus previous MI. There was no significant difference between the two groups. A cohort of 105 asymptomatic Afro-Caribbeans showed a much reduced frequency of the polymorphism.
Black People↗
[The polymorphism of the angiotensin I-converting enzyme gene and its association with ischemic cardiopathy].
The role played by angiotensin in the development of coronary heart disease is a subject of increasing interest. This interest is due to the results of several trials suggesting that treatment with angiotensin I-converting enzyme inhibitors decrease the incidence of clinical manifestations of coronary heart disease. The relationship between angiotensin and coronary heart disease is being analyzed both from basic and clinical approaches. As a result of such investigations, a polymorphism in the angiotensin converting enzyme gene has been described and the role of this polymorphism as a possible risk factor for coronary heart disease has been reported. In this paper the current knowledge about the angiotensin-converting enzyme gene is reviewed and its relationship with coronary heart disease is discussed.
Humans↗
Angina pectoris and normal coronary arteriograms: clinical presentation and hemodynamic characteristics.
Up to 30% of patients undergoing coronary angiography for the assessment of chest pain suggestive of coronary artery disease have "normal" studies. Several reports have indicated that a proportion of patients with angina and normal coronary arteriograms have reduced coronary flow reserve. The interpretation of these findings is, however, controversial as the majority of patients do not have definitive evidence for myocardial ischemia and have a good long-term prognosis. The clinical presentation of patients with angina and normal coronary arteriograms differs in different series and this may be just a reflection of the heterogeneous nature of the syndrome. A diversity of pathogenetic mechanisms have been postulated to explain "syndrome X" (chest pain and normal coronary arteriograms) but little is known at present about the true nature of the syndrome. The present article discusses the clinical and hemodynamic features of this intriguing disorder with particular reference to patients with syndrome X and microvascular angina.
Angina Pectoris↗
Rapid angiographic progression of coronary artery disease in patients with angina pectoris. The role of complex stenosis morphology.
BACKGROUND: Rapid disease progression commonly underlies acute coronary events, and "complex" stenosis morphology may play a role in this phenomenon. METHODS AND RESULTS: We studied the role of complex stenosis morphology in rapid disease progression in 94 consecutive patients awaiting routine coronary angioplasty. Coronary arteriography was repeated at 8 +/- 3 months' follow-up, immediately preceding angioplasty (68 patients) or after an acute coronary event (26 patients). Disease progression of 217 stenoses, of which 79 (36%) were "complex" and 138 (64%) were "smooth," was assessed by computerized angiography. At presentation, 63 patients had stable angina pectoris and 31 had unstable angina that settled rapidly with medical therapy. At follow-up, 23 patients (24%) had progression of preexisting stenoses and 71 (76%) had no progression. Patients with progression were younger (55 +/- 12 years) than those without (58 +/- 9 years) but did not differ with regard to risk factors, previous myocardial infarction, or severity and extent of coronary disease. Twenty-three lesions (11%) progressed, 15 to total occlusion (11 complex and 4 smooth; 65%). Progression occurred in 17 of the 79 complex stenoses (22%) and in 6 of the 138 smooth lesions (4%) (P = .002). Mean stenosis diameter reduction was also significantly greater in complex than in smooth lesions (11.6% versus 3.9% change; P < .001). Acute coronary events occurred in 57% of patients with progression compared with 18% of those without progression (P < .001) and were more frequent in patients who presented with unstable angina (P = .002). CONCLUSIONS: Rapid stenosis progression is not uncommon, and complex stenoses are at risk more than smooth lesions.
Angina Pectoris↗
Angiographic stenosis progression and coronary events in patients with 'stabilized' unstable angina.
BACKGROUND: Recent studies suggest that angiographically complex coronary stenoses are associated with an adverse short-term outcome. It is not known, however, if this applies to unstable angina patients who stabilize on medical therapy. METHODS AND RESULTS: We prospectively studied 85 consecutive patients with unstable angina who stabilized on medical therapy but were found to require angioplasty for treatment of obstructive coronary disease. Angiography was carried out at admission, and patients were restudied 8 +/- 4 months (mean +/- SD) after the first angiogram. Ischemia-related stenoses were identified and classified as "complex" (irregular borders, overhanging edges, or thrombus) or "smooth" (absence of complex features). Stenosis progression (> or = 20% diameter reduction or new total occlusion) was assessed by automated edge detection. At initial angiography, there were 198 stenoses (> or = 50%, 102), of which 85 (54 complex and 31 smooth) were ischemia related. At restudy, 21 ischemia-related stenoses and 8 non-ischemia-related stenoses progressed (25% versus 7%, P = .001). Seventeen of the 21 ischemia-related stenoses that progressed developed into total occlusion compared with 3 of the 8 non-ischemia-related stenoses (P = .02). Changes in average stenosis severity and in absolute stenosis diameter were significantly larger in ischemia-related stenoses than in non-ischemia-related stenoses (P = .03). Eighteen (34%) complex stenoses progressed, compared with 3 (10%) smooth lesions (P = .02). During follow-up, 1 patient died (myocardial infarction) and 25 patients had nonfatal coronary events that were associated with progression of ischemia-related stenoses in 14 (56%). CONCLUSIONS: In unstable angina patients who stabilize medically, subsequent short-term stenosis progression and coronary events are common. The unstable coronary lesion (particularly complex stenoses) is often not stabilized and will continue to progress over the ensuing months.
Angina, Unstable↗