Epicardial Coronary Arteries In Patients Research Articles

Degrees of Cross-Sectional-Area Luminal Narrowing of the Four Major Epicardial Coronary Arteries in Patients With Otherwise Functionally and Anatomically Normal Hearts

Described herein are necropsy findings in the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries in 86 patients aged 10-70 years who never had symptoms of myocardial ischemia, and at autopsy had otherwise anatomically normal hearts. All 86 died of a non-cardiovascular condition. In each of these patients all 4 major epicardial coronary arteries were excised intact from the heart, divided into 5-mm segments, and each segment prepared for histologic examination. The degrees of cross-sectional area (CSA) narrowingwere determined from histologic examination of each 5-mm segment. The degree of narrowing in each 5 mm segment was divided into 4 categories: 0% to 25%, 26% to 50%, 51% to 75%, and 76% to 100%. Twelve patients (14%) had ≥1 artery narrowed >75% in CSA, a single artery in 9 patients, and 2 arteries in each of 3 patients. In contrast to the relative infrequency of narrowing >75%, narrowing 51-75% was common, and was present in 36 (42%) of the 86 patients. Of the 258 major coronary arteries (excludes the left main) studied in the 86 patients, 15 (6%) were narrowed >75%, and 70 (24%) were narrowed 51% to 75% in CSA. Even mild narrowing (26% to 50%) of the left main coronary artery (66 patients) was generally accompanied by 51% to 75% or greater narrowing of at least one of the other major coronary arteries. In conclusion, even hearts which have functioned normally and are otherwise anatomically normal, usually have some degree of atherosclerotic plaque in the major epicardial coronary arteries.

Morphometry and hemodynamics of coronary artery aneurysms caused by atherosclerosis

Background and aimsAtherosclerosis is the first etiology of coronary artery aneurysm (CAA). It is, however, challenging to inhibit the development of CAA. The aim of the study is to carry out morphometric and hemodynamic analyses in epicardial coronary arteries of patients with CAAs caused by atherosclerosis. MethodsVarious morphometric parameters were obtained from the reconstructed epicardial coronary arterial trees of 61 patients and multiple hemodynamic parameters were determined from the computed flow fields. A two-step analysis method was proposed to enhance the risk assessment of CAAs, i.e., coronary artery bifurcation is the major risk factor for CAA followed by high aneurysm shape index (L/W, where L and W refer to the aneurysm length and maximum diameter, respectively). ResultsPatients with CAA covering a bifurcation have the higher occurrence (71% and 55% for L/W ≥ 2 and L/W < 2, respectively) of myocardial ischemia relevant to abnormal hemodynamic parameters in comparison with those with CAA in one vessel (43% and 40% for L/W ≥ 2 and L/W < 2, respectively). Patients with CAA of L/W ≥ 2 covering a bifurcation show the worst hemodynamic environment. ConclusionsMorphometric and hemodynamic studies support the two-step analysis method, which provides a clinical rationale for the noninvasive assessment of CAAs.

Quantitative Extent of Atherosclerotic Plaque in the Major Epicardial Coronary Arteries in Patients with Fatal Coronary Heart Disease, in Coronary Endarterectomy Specimens, in Aorta-Coronary Saphenous Venous Conduits, and Means to Prevent the Plaques: A Review after Studying the Coronary Arteries for 50 Years

This review tries to answer the following 15 questions: Is atherosclerosis a systemic or a regional disease? Is atherosclerosis in any particular region focal or diffuse? What is the quantity of atherosclerotic plaques in endarterectomy specimens of the right coronary artery in patients undergoing coronary artery bypass grafting (CABG) compared to that in the right coronary artery in patients with fatal coronary artery disease? How do the units used for measuring arterial narrowing by angiography compare to the units used for measuring arterial narrowing at necropsy? What do atherosclerotic plaques consist of in coronary arteries in patients with fatal coronary disease? What is the quantity of atherosclerotic plaque in bypassed -vs- non-bypassed native coronary arteries in patients dying early (<60 days) or late (>60 days) after coronary artery bypass grafting? What is the frequency of acute coronary lesions and multi-luminal channels at necropsy in patients with unstable angina pectoris, sudden coronary death, and acute myocardial infarction? What is the mechanism of luminal widening by angioplasty in the coronary arteries? What observations suggest that atherosclerotic plaques are the result at least in part of organization of thrombi? Is atherosclerosis a multifactoral or a unifactoral disease? What characteristics distinguish carnivores and herbivores? What are reasonable guidelines for whom to treat with lipid-altering agents? What is the rule of 5 and the rule of 7 in statin therapy? What is the effect of lipid lowering drug therapy on coronary luminal narrowing? What are some requisites for a healthy life?

Frequency of Non Obstructive Epicardial Coronary Arteries in Patients with Typical Cardiac Chest Pain

Frequency of Non Obstructive Epicardial Coronary Arteries in Patients with Typical Cardiac Chest Pain

P839Lectin-like oxidized low density lipoprotein receptor-1 exhibits increased expression in the epicardial coronary arteries in patients with coronary artery disease. The intramyocardial paradox

P839Lectin-like oxidized low density lipoprotein receptor-1 exhibits increased expression in the epicardial coronary arteries in patients with coronary artery disease. The intramyocardial paradox

Tortuosity, Recurrent Segments, and Bridging of the Epicardial Coronary Arteries in Patients With the Takotsubo Syndrome

Myocardial bridging (MB) and a long recurrent wraparound left anterior descending artery (wrap-LAD) are coronary anatomic variants that have been recently suggested to be associated with takotsubo syndrome (TS). Until now, coronary artery tortuosity (CAT) has never been investigated in this setting. Our study sought to evaluate the prevalence of the aforementioned anatomic variants in a large population with TS. In this retrospective angiographic study, 109 patients with TS were compared with 109 age- and gender-matched subjects without coronary artery disease, valve heart disease, or cardiomyopathy. CAT was identified by ≥3 consecutive curvatures ≥90° (criteria 1) or by ≥2 consecutive curvatures ≥180° (criteria 2). Wrap-LAD was defined if any part of the vessel outreached the apex of the left ventricle and MB as the presence of a milking effect or a step-up and step-down phenomenon. An anatomic variant was found in 79 patients with TS (72%) and in 48 controls (44%) (p <0.001). CAT in at least 1 vessel (criteria 1: 49% vs 20%, p <0.001; criteria 2: 38% vs 13%, p <0.001), ≥2 vessels (criteria 2: 14% vs 3%, p= 0.005), and wrap-LAD (41% vs 27%, p= 0.02) were significantly more frequent in patients with TS than in controls. The prevalence of MB (9% vs 5%, p= 0.18) did not differ between groups. In conclusion, CAT and wrap-LAD have higher prevalence in patients with TS than in matched controls. These findings could support the hypothesis that anatomic variants might act as potential pathogenic substrates in TS.

Microvascular Obstruction Evaluation Using Cardiovascular Magnetic Resonance (CMR) in ST-Elevated Myocardial Infarction (STEMI) Patients.

SummaryBackroundRestoration of blood flow in epicardial coronary artery in patients with acute myocardial infarction can, but does not have to restore efficient blood flow in coronary circulation.The aim of the study was a direct comparison of microvascular obstruction (MVO) detected by rest and stress perfusion imaging and gadolinium enhancement obtained 2 min. (early MVO) and 15 min. (delayed MVO) post contrast.Material/Methods106 patients with first anterior myocardial infarction were studied. Cardiovascular magnetic resonance (CMR) was performed 5±2 days after primary percutaneous coronary intervention (pPCI). Stress and rest perfusion imaging was performed as well as early and delayed gadolinium enhancement and systolic function assessment.Scoring of segmental function, perfusion defect, MVO and scar transmurality was performed in 16 segment left ventricular model.ResultsThe prevalence of MVO varies significantly between imaging techniques ranging from 48.8% for delayed MVO to 94% with stress perfusion. Median sum of scores was significantly different for each technique: stress perfusion 13 (7; 18), rest perfusion 3 (0.5; 6), early MVO 3 (0; 8), delayed MVO 0 (0; 4); p<0.05.Infarct size, stress and rest perfusion defects were independent predictors of LV EF at discharge from hospital.ConclusionsImaging protocol has a significant impact on MVO results. The study is the first to describe a stress-induced MVO in STEMI patients. Further research is needed to evaluate its impact on a long term prognosis.

Assessment of Coronary Flow with Transthoracic Color Doppler Echocardiography in Patients with Hypertrophic Cardiomyopathy

Recent advances in echocardiography have allowed assessment of flow velocity in the epicardial coronary arteries of patients with ischemic heart disease, using transthoracic color Doppler echocardiography (TTDE). However, few data are available regarding coronary blood flow in patients with hypertrophic cardiomyopathy (HCM). To assess the epicardial coronary arteries of patients with HCM. A group of 25 patients with HCM was assessed prospectively (mean age 57±21years, 11 male) using TTDE; flow velocities in the epicardial coronary arteries were measured and compared with those obtained in 10 age- and gender-matched controls. Analysis of the diastolic spectral waveform included flow velocity integral (VTI), peak velocity, deceleration time, and deceleration slope measurements, while systolic waveform analysis included peak flow measurement and morphology assessment (positive, absent or negative). An analysis of variance (ANOVA) test was used for multiple comparisons for variables with a normal distribution, and a Kruskal-Wallis test was used for variables with non-Gaussian distribution. Patients with HCM exhibited an increase in diastolic flow velocity with a rapid deceleration slope and a systolic slope which was decreased, absent or reversed, compared to normal subjects. On linear regression analysis there was no correlation with the type of hypertrophy or magnitude of the intraventricular pressure gradient in patients with obstructive HCM. In patients with HCM, noninvasive assessment with TTDE revealed abnormal findings in the distal flow of the epicardial coronary arteries, very similar to those seen in the no-reflow phenomenon. These findings were independent of the type of hypertrophy and magnitude of the intraventricular pressure gradient in patients with obstructive HCM.

Evaluation of coronary microvascular function in patients with vasospastic angina

To investigate endothelium-dependent and -independent coronary microvascular functions in patients with vasospastic angina (VSA). Thirty-six patients with VSA (30 men and 6 women; mean age, 58 years) were enrolled in this study. VSA was defined as ≥ 90% narrowing of the epicardial coronary arteries on angiography performed during a spasm provocation test, presence of chest pain, and/or ST-segment deviation on an electrocardiogram (ECG). Patients (n = 36) with negative spasm provocation test results and those matched for age and sex were enrolled as a control group (nonVSA group). Low-dose acetylcholine (ACh; 3 μg/min) was infused into the left coronary ostium for 2 min during the spasm provocation test. Following the spasm provocation test, nitroglycerin (0.2 mg) was administered intracoronally. Coronary blood flow (was calculated from quantitative angiography and Doppler flow velocity measurements, and the coronary flow reserve was calculated as the ratio of coronary flow velocity after injection of adenosine triphosphate (20 μg) to the baseline value. Changes in the coronary artery diameter in response to ACh and nitroglycerin infusion were expressed as percentage changes from baseline measurements. Body mass index was significantly lower in the VSA group than in the nonVSA group. The frequency of conventional coronary risk factors and the rate of statin use were similar between the 2 groups. The left ventricular ejection fraction as evaluated by echocardiography was similar between the 2 groups. The duration of angina was 9 ± 2 mo. The results of blood chemistry analysis were similar between the 2 groups. Low-dose ACh did not cause coronary spasms. The change in coronary artery diameter in response to ACh was lower in the VSA group (-1.4% ± 9.3%) than in the nonVSA group (3.1% ± 6.5%, P < 0.05), whereas nitroglycerin-induced coronary artery dilatation and coronary blood flow increase in response to ACh or coronary flow reserve did not differ significantly between the 2 groups. These findings suggest that microvascular coronary function may be preserved despite endothelial dysfunction of the epicardial coronary arteries in patients with VSA.

Diagnostic Accuracy of Cardiac Positron Emission Tomography Versus Single Photon Emission Computed Tomography for Coronary Artery Disease

Background— Positron emission tomography (PET) myocardial perfusion imaging (MPI) offers technical benefits compared with single photon emission computed tomography (SPECT) MPI, but there has been no systematic comparison of their diagnostic accuracy for coronary artery disease. We performed a bivariate meta-analysis of the published literature to compare the sensitivity and specificity of PET versus SPECT stress MPI for ≥50% stenosis of any epicardial coronary artery in patients with known or suspected coronary artery disease. Methods and Results— We searched MEDLINE and EMBASE from inception through January 2012 and the references of identified studies for prospective, English language studies that evaluated the sensitivity and specificity of PET and/or SPECT MPI with coronary angiography as the reference standard and reported sufficient data to calculate patient-level true and false positives and negatives. Two investigators independently extracted patient and study characteristics; a third investigator resolved any disagreements. We identified 117 studies, including 108 evaluating SPECT MPI, 4 evaluating PET MPI, and 5 evaluating both modalities. Bivariate meta-analysis demonstrated a significantly higher pooled mean sensitivity with PET (92.6% [95% Confidence Interval, 88.3% to 95.5%]) compared with SPECT (88.3% [95% confidence interval, 86.4% to 90.0%]) ( P =0.035). No significant difference in specificity was observed between PET (81.3% [95% confidence interval, 66.6% to 90.4%]) and SPECT (75.8% [95% confidence interval, 72.1% to 79.1%]) ( P =0.39). Few studies investigated coronary angiography with PET. Only 5 studies directly compared SPECT and PET. Conclusions— In a meta-analysis of 11,862 patients, PET MPI demonstrated a higher sensitivity for coronary artery disease than SPECT MPI. No difference in specificity was detected in the pooled analysis of PET and SPECT MPI.

Myocardial Bridging

According to postmortem studies, coronary atherosclerosis can be substantial and reach a high prevalence of advanced lesions, including atheroma and fibroatheroma in young adults.1,2 Risk factors associated with coronary atherosclerosis such as dyslipidemia, smoking, diabetes mellitus, and hypertension have been identified. The development of atherosclerosis seems to be related to the magnitude and duration of exposure.3 Although research concentrates on identifying genetic markers in genome-wide association studies, there is still a lack of knowledge about the individual risk of developing coronary atherosclerosis.4 When atherosclerosis presents as acute coronary syndromes, mortality may be high.5 Plaque rupture and erosion have been identified as major underlying pathological-anatomic characteristics,6 but some suspect other mechanisms.7 In this issue of Circulation , Ishikawa et al8 present evidence that myocardial bridging may play a role as a congenital anatomic risk factor for coronary atherosclerosis and myocardial infarction. Article see p 376 Myocardial bridging results when myocardial tissue covers part of the left anterior descending coronary artery, resulting in a tunneled arterial segment, which can be regarded as a congenital variant.9–11 The prevalence is reported to be >50% at autopsy.12 Clinically, the diagnosis of myocardial bridging is established by coronary angiography demonstrating a systolic compression, described as a “milking effect,”13 but it was present in only <5% of cases recently in a large number of Chinese patients.14 When nitroglycerin was used as …

Deposition of amyloid proteins in the epicardial coronary arteries of 58 patients with primary systemic amyloidosis

We sought to determine the distribution and the effect of amyloid on epicardial coronary arteries in patients with primary cardiac amyloidosis. We reviewed pathologic specimens taken after autopsy or cardiac transplantation from 58 patients with primary cardiac amyloidosis. Patients were seen from 1981 to 2000. Multiple sections of epicardial coronary arteries (left anterior descending artery, left circumflex artery, and right coronary artery) were examined to determine the degree of amyloid deposition in the intima, media, adventitia, and vasa vasorum (vasa vasorum are nutrient arteries for the coronary arteries themselves). In 56 of 58 patients (97%), amyloid was present in epicardial coronary arteries. Amyloid was identified in all artery layers (intima, media, and adventitia), and more patients had amyloid in the adventitia. However, amyloid did not cause intraluminal obstruction of epicardial coronary arteries in any patient. The vasa vasorum had considerable deposits and, in many patients, were obstructed by amyloid. Patients with obstruction of the vasa vasorum were significantly more likely to have obstructive intramural coronary amyloidosis than patients without vasa vasorum obstruction (P=.002). The epicardial coronary arteries of patients with primary cardiac amyloidosis had extensive amyloid deposition. This deposition, however, did not lead to obstruction of epicardial coronary arteries and therefore did not contribute to ischemic syndromes observed in these patients. Obstruction of the vasa vasorum was associated with obstructive intramural coronary amyloidosis.

Angiotensin receptor antagonist losartan improves endothelial function of epicardial coronary arteries in patients with essential hypertension.

Angiotensin II can impair endothelial function, which is mediated by the angiotensin II type 1 receptor subtype. The study sought to determine whether treatment with the angiotensin II type 1 receptor antagonist losartan would restore the normal dilation of the left main coronary artery (LMCA) by cold pressor test in patients with essential hypertension, as shown by echocardiography. The study population included 30 patients with mild to moderate essential hypertension and 30 matched healthy subjects. Measurements of the cold pressor test-induced and nitroglycerin-induced changes in LMCA diameter by echocardiography were performed at the end of the washout period and after 12 weeks of losartan administration. The percent change in LMCA diameter induced by the cold pressor test in hypertensive patients (-3.5 +/- 8.8%) was significantly lower than that in control subjects (10.2 +/- 3.7%, p<0.0001). After losartan treatment, the percent change (13.9 +/- 8.4%) was significantly higher than that before losartan treatment (-3.5 +/- 8.8%, p < 0.0001), but not significandy different between the 17 hypertensive patients with satisfactory control of blood pressure (13.8 +/- 9.1%) and the 13 hypertensive patients without satisfactory control of blood pressure (14.0 +/- 7.7%, p = 0.9). Losartan treatment in patients with essential hypertension did not modify the percent change in LMCA diameter caused by sublingual administration of nitroglycerin (23.2 +/- 14.0% vs. 27.3 +/- 13.7%, p = 0.2). This study demonstrates that treatment with losartan normalized response of the LMCA to the cold pressor test in patients with mild to moderate essential hypertension and that this effect is not dependent on the reduction of blood pressure.

L -Arginine and Thrombosis

HomeCirculationVol. 104, No. 25l-Arginine and Thrombosis Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBl-Arginine and Thrombosis Dimitris Tousoulis, MD PhD, Costas Tentolouris, MD and Pavlos Toutouzas, MD Dimitris TousoulisDimitris Tousoulis Cardiology Unit, Athens University Medical School, Athens, Greece Search for more papers by this author , Costas TentolourisCostas Tentolouris Cardiology Unit, Athens University Medical School, Athens, Greece Search for more papers by this author and Pavlos ToutouzasPavlos Toutouzas Cardiology Unit, Athens University Medical School, Athens, Greece Search for more papers by this author Originally published17 Dec 2001https://doi.org/10.1161/circ.104.25.e159Circulation. 2001;104:e159To the Editor:Kapostza et al1 reported that the administration of l-arginine (the precursor of nitric oxide synthesis) after surgery resulted in a highly significant reduction in the frequency of embolic signals after carotid endarterectomy in patients who were already being treated with aspirin and heparin. Patients with carotid artery disease usually suffer from coronary atherosclerosis. Therefore, it would be useful to know the impact of l-arginine administration on advanced coronary artery atherosclerosis.We examined,2,3 by quantitative angiography, the vasomotor effects of an intracoronary infusion of l-arginine in epicardial coronary artery segments and in coronary stenoses in patients with coronary artery disease and stable angina. We found that proximal coronary segments and coronary stenoses dilated in response to acute intracoronary administration of l-arginine. The greatest response to l-arginine was at the site of severe coronary stenoses. Moreover, we have shown that stenoses with a complex morphology show a greater dilation compared with those of smooth morphology, whether concentric or eccentric.3 This finding is consistent with stimulation of nitric oxide synthase activity by l-arginine administration. It provides further evidence of preserved nitric oxide synthase activity at the site of coronary stenoses, particularly within stenoses with complex morphology.4 Furthermore, because this effect was also found in nonstenotic segments of diseased coronary arteries, it is either a physiological or a pathological response requiring only minimal coronary disease.Our findings suggest that l-arginine supplementation may have a beneficial effect on diseased epicardial coronary arteries in patients with stable angina. In addition, a recent study5 showed that local l-arginine delivery after balloon angioplasty reduces monocyte binding and induces apoptosis and, therefore, may be beneficial for restenosis. The actions of l-arginine are complex, and the responses of epicardial coronary arteries and carotid arteries to l-arginine may be different. Therefore, further studies are needed to elucidate the impact of l-arginine on atherosclerosis and thrombosis in different parts of the arterial tree. The l-arginine intravenously administered may reduce the embolic signals and dilate coronary stenoses in patients with carotid and coronary artery disease.1 Kaposzta Z, Baskerville PA, Madge D, et al. l-arginine, and S-nitrosoglutathione reduce embolization in humans. Circulation. 2001; 103: 2371–2375.CrossrefMedlineGoogle Scholar2 Tousoulis D, Davies G, Tentolouris C, et al. Coronary stenosis dilatation induced by l-arginine. Lancet. 1997; 349: 1812–13.CrossrefMedlineGoogle Scholar3 Tousoulis D, Davies GJ, Tentolouris C, et al. Vasomotor effects of L- and D-arginine in stenotic atheromatous coronary plaque. Heart. 2001; 86: 296–301.CrossrefMedlineGoogle Scholar4 Goumas G, Tentolouris C, Tousoulis D, et al. Therapeutic modification of the l-arginine-eNOS pathway in cardiovascular diseases. Atherosclerosis. 2001; 154: 255–267.CrossrefMedlineGoogle Scholar5 Niebauer J, Schwarzacher SP, Hayase M, et al. Local l-arginine delivery after balloon angioplasty reduces monocyte binding and induces apoptosis. Circulation. 1999; 100: 1830–1835.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited ByTweddell J, Hoffman G, Mussatto K, Fedderly R, Berger S, Jaquiss R, Ghanayem N, Frisbee S and Litwin S (2002) Improved Survival of Patients Undergoing Palliation of Hypoplastic Left Heart Syndrome: Lessons Learned From 115 Consecutive Patients, Circulation, 106:12_suppl_1, (I-82-I-89), Online publication date: 24-Sep-2002. December 17, 2001Vol 104, Issue 25 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.104.25.e159PMID: 11748124 Originally publishedDecember 17, 2001 PDF download Advertisement

Vitamin C improves endothelial function of epicardial coronary arteries in patients with hypercholesterolaemia or essential hypertension--assessed by cold pressor testing.

There is evidence that formation of free radicals increases in patients with hypertension or hypercholesterolaemia, which may contribute to endothelial dysfunction of epicardial coronary arteries due to inactivation of the vasodilator NO. The present study was designed to test whether the abnormal constriction of epicardial coronary arteries due to sympathetic stimulation by the cold pressor test in patients with essential hypertension or hypercholesterolaemia could be reversed by administration of the antioxidant vitamin C. In 28 patients without relevant coronary artery stenosis the cold pressor test was performed before and after a 3 g infusion of vitamin C. In five normal controls the cold pressor test led to a similar increase in luminal area before and after vitamin C (3.7+/-1.3% and 1.9+/-0.8%, ns vs before vitamin C). In nine hypercholesterolaemic patients the cold pressor test led to a -14.1+/-2.8% reduction in cross-sectional area before vitamin C. This constriction was significantly improved after vitamin C to -7.6%+/-2.0, P=0.027 vs before vitamin C. In nine hypertensive patients, the cold pressor test led to a -17.1+/-3.2% decrease in cross-sectional area before vitamin C, which was improved to -7.1+/-3.1 after vitamin C, P=0.004 vs before vitamin C. This increase in luminal area was significant in each group in comparison with normal controls (each P<0.05). Administration of saline (placebo group, five patients) had no significant effect on cold pressor test-induced constriction (-6.9+/-3.9% before and -6. 8+/-3.7% after saline). The antioxidant vitamin C reverses cold pressor test-induced vasoconstriction of epicardial coronary arteries in patients with hypertension or hypercholesterolaemia. Our data suggest that enhanced oxidative stress contributes to impaired endothelial function in this patient population.

Evidence of partially preserved endothelial dilator function in diseased coronary arteries

OBJECTIVETo examine the effects of substance P (endothelium dependent vasodilator) and glyceryl trinitrate (endothelium independent vasodilator) on epicardial coronary arteries in patients with normal coronary angiograms and patients with coronary...

Enhanced coronary vasoconstriction after PTCA in patients with acute ischemia.

Coronary vasoconstriction of the distal vessel segment has been reported after percutaneous transluminal coronary angiography (PTCA), which was explained by increased vasoconstrictor influences. In patients with acute ischemia these changes may be even enhanced. Thus, vasomotion of the epicardial coronary arteries was studied before and after PTCA in patients with acute ischemia due to unstable angina or acute infarction. 52 patients were divided into 2 groups: Group 1 (controls) consisted of 31 patients who underwent elective (PTCA) and group 2 of 21 patients who underwent emergency PTCA for unstable angina or acute infarction. Coronary artery dimensions proximal and distal to the culprit lesion were determined by quantitative coronary angiography before and after PTCA as well as after 0.2 mg nitroglycerin i.c. at the end of the procedure. Stenosis severity was similar before and after PTCA in both groups (before, 91 +/- 8% in group 1 vs 90 +/- 9% in group 2; after, 28 +/- 9% vs 23 +/- 10%, resp.). Heart rate and mean blood pressure remained unchanged. In the group with acute ischemia no vasodilation of the proximal (2 +/- 3%) and distal vessel (-1 +/- 4%) occurred after PTCA, whereas in the control group significant vasodilation of both vessel segments (11 +/- 2% resp. 13 +/- 3%) was found. The response to nitroglycerin was maintained in both groups. In the control group there was a significant correlation between stenosis severity and percent diameter change of the distal vessel segment. However, in the acute ischemic group this relationship was shifted downwards suggesting an enhanced vasoconstrictor response in these patients. Epicardial coronary arteries in patients with acute ischemia show an enhanced vasoconstriction after PTCA. Nevertheless, the response to nitroglycerin is maintained suggesting that functional (endothelial dysfunction) rather than structural factors are responsible for this phenomenon.

Hemodynamic and Coronary Effects of the Endothelin Antagonist Bosentan in Patients With Coronary Artery Disease

Endothelin is a potent endothelium-derived vasoconstrictor peptide with proliferative properties. Elevated levels of the peptide occur in coronary artery disease; however, its pathophysiological role as a regulator of coronary tone and structure is uncertain. Endothelin-receptor antagonists are specific tools to clarify this issue and might be useful in the treatment of coronary artery disease. In a double-blind, placebo-controlled randomized study, we investigated the effects of the ETA/ETB endothelin-receptor antagonist bosentan or placebo on systemic and coronary hemodynamics in 28 patients with angiographically documented stable coronary artery disease by quantitative coronary angiography and an intracoronary Doppler guidewire. Bosentan 200 mg IV decreased systolic blood pressure (P<0. 05), whereas heart rate increased slightly (P<0.05). Coronary diameter increased, particularly in vessels with no or mild angiographic changes (P<0.01). Glycerol trinitrate did not further dilate these segments, whereas coronary diameter increased significantly after nitrate in the placebo group. The increase in coronary diameter after bosentan correlated inversely with plasma LDL-cholesterol levels (P<0.01) in both stenotic and angiographically normal coronary segments. Coronary flow velocity did not change. Bosentan was well tolerated. Endogenous endothelin exerts a vasoconstrictor tone in epicardial coronary arteries of patients with coronary artery disease, as evidenced by the vasodilation exerted by the combined ETA/ETB endothelin-receptor antagonist bosentan under acute conditions. Bosentan can safely be given to these patients. Hence, further long-term studies are necessary to determine the therapeutic potential of endothelin-receptor antagonists in patients with coronary artery disease.

Evidence of endothelial dysfunction of epicardial coronary arteries in patients with immunohistochemically proven myocarditis

Background Recent reports indicate that myocarditis can be associated with acute myocardial ischemia and even myocardial infarction in patients with normal arteriograms. We therefore tested the hypothesis that patients with biopsy-proven myocarditis have endothelial dysfunction despite angiographically smooth epicardial coronary arteries. Methods and Results Graded concentrations of the endothelium-dependent vasodilator acetylcholine (10 -6 to 10 -4 mol/L) and for comparison, the non-endothelium-dependent vasodilator nitroglycerin (0.3 mg intracoronary), were infused into the left coronary arteries of 18 patients (mean age 47 ± 9 years, 8 women and 10 men) with biopsy-proven myocarditis but without angiographically demonstrable coronary artery disease. Vascular responses were analyzed by quantitative coronary angiography. Three patients had an intact vasodilator response to acetylcholine concentrations of up to 10 -4 mol/L in all segments of the left coronary artery, with a mean dilatation of +9.9% ± 2%. In contrast, paradoxical constriction by acetylcholine occurred in 9 patients, who showed a mean change in coronary artery diameter of –11% ± 3%. Six patients had no significant change in any segments in response to acetylcholine (–2.5% ± 4%). There was a significant inverse correlation between the number of T-lymphocytes in the myocardium and the response of the epicardial coronary arteries to acetylcholine (Pearson correlation coefficient –0.49, P = .03). Conclusions It can be assumed that the process of myocarditis is associated with impairment of endothelium-dependent vasodilation in response to acetylcholine in most patients. Vasoconstriction in the presence of acetylcholine in myocarditis is likely to reflect an abnormality of endothelial function. Endothelial dysfunction of coronary arteries may explain the occurrence of myocardial ischemia in patients with myocarditis. (Am Heart J 1998;136:389-97.)

Importance of left anterior descending coronary artery curvature in determining cross-sectional plaque distribution assessed by intravascular ultrasound

We assessed the relation between the circumferential distribution of coronary atherosclerotic plaques and the structure of the epicardial coronary arteries in patients with coronary artery disease using intravascular ultrasound in vivo. Coronary atherosclerosis preferentially formed at the inner arc of the curved coronary vessels, and greater vessel curvatures were associated with greater distributions of atherosclerotic lesions along the inner coronary artery wall.