The relationship between growth of atherosclerotic plaques, variant angina and sudden death

Clinico-pathological findings are described in two patients with typical variant angina who died suddenly during an ischemic attack. In both cases, detailed pathologic examination of the coronary arteries disclosed severe focal atherosclerosis of the anterior descending coronary artery. The only distinctive histological finding was new intimal proliferation of smooth muscle cells enmeshed within mucoid substance, superimposed on the old fibrous cap of the plaque. These findings agree with experimental and clinical data which suggest that coronary vasospasm may be related to growth of atherosclerotic plaques. This study provides histological evidence that progression of an atherosclerotic plaque may underlie variant angina and sudden death.     

Coronary spasm masquerading as progressive exertional angina with normal coronaries

A case of typical exertional angina secondary to chronic focal vasospasm with normal coronary arteries and the role of vasospasm in typical angina are briefly discussed. Recommendations are made regarding evaluation of patients with normal coronaries and angina.     

Histological evaluation of coronary plaque in patients with variant angina: relationship between vasospasm and neointimal hyperplasia in primary coronary lesions

Objectives. This study was designed to determine whether coronary vasospasm in patients with variant angina pectoris (VAP) may produce focal organic lesions at the site of vasospasm that would contribute to disease progression.Background. Recent clinical angiographic and experimental studies have demonstrated the potential role of vasospasm in the worsening of organic coronary stenosis.Methods. We studied histologically the coronary plaques obtained at atherectomy in 202 patients with moderate to severe coronary stenosis. This population included 22 patients with VAP, 100 patients with chronic stable angina and 80 patients with restenosis following angioplasty or atherectomy. Diagnosis of VAP was based on both the clinical feature of angina at rest associated with ST elevation and a positive response to acetylcholine provocation test.Results. The most common histological appearance in 92% of patients with stable angina was hypocellular fibroatheromatous plaques, whereas neointimal hyperplasia was the characteristic feature of the plaque observed in 90% of patients with restenosis. The coronary specimens at the site of spasm in 15 of the 22 patients (68%) with VAP demonstrated intimal injuries such as neointimal hyperplasia (15), thrombus formation (2), and intimal hemorrhage (3). Neointimal hyperplasia was significantly more common in the patients with VAP as compared with those with stable angina (68% vs. 8%; p < 0.0001). A rapid progression of organic stenosis within three years was angiographically found in 5 of the 22 patients with variant angina. In all five cases, neointimal hyperplasia was the main contributor to the worsening of the organic lesion at the site of spasm. These histological findings in patients with VAP extremely resembled those in restenosis. Except for vasospasm, no factors significantly predicted the presence of neointimal formations in primary coronary lesions.Conclusions. Coronary vasospasm may provoke vascular injury that leads to the formation of neointima in VAP patients similar to that seen with restenosis. Coronary spasm may thus play a key role in the rapid coronary stenosis progression in certain patients with VAP.     

Frequency and distribution of thin-cap fibroatheroma and ruptured plaques in human coronary arteries: a pathologic study.

OBJECTIVES: Our purpose was to quantify the frequency and distribution of suspected vulnerable lesions, defined as thin-capped fibroatheroma (TCFA) and ruptured plaque, in human coronary artery autopsy specimens. BACKGROUND: Most acute coronary events and sudden death are believed to arise from rupture of a TCFA followed by thrombosis. Although there is general agreement that clinical events are usually caused by focal lesions, there is considerable debate over the relative importance of focal versus systemic factors in the pathogenesis of atherosclerosis. METHODS: We longitudinally sectioned coronary arteries from 50 whole hearts taken from patients (mean age 73 years, 64% men) dying of cardiovascular (n = 33), noncardiovascular (n = 13), and unknown (n = 4) causes. A total of 3,639 longitudinal segments of length 3 mm were sectioned from 148 arteries, accounting for 10.9 m of total tissue length. Specimens were classified on the basis of histology and computer-aided morphometry. RESULTS: Twenty-three TCFA and 19 ruptured plaques were found (mean +/- SD: 0.46 +/- 0.95 and 0.38 +/- 0.70 per heart, respectively), and these lesions accounted for only 1.6% and 1.2%, respectively, of the total length of the coronary tree examined in patients dying of cardiovascular causes. The majority of TCFA and ruptured plaque localized in the proximal third of the major coronary arteries, and in 92% of cases these lesions clustered within 2 or fewer nonoverlapping 20-mm segments. CONCLUSIONS: The suspected precursors of rupture-mediated thrombosis occur in a limited, focal distribution in the coronary arteries.     

Multivessel coronary vasospasm mimicking triple-vessel obstructive coronary artery disease

Spontaneous coronary artery spasm is an important cause of morbidity both in patients with atherosclerotic coronary artery disease and in those with Prinzmetal's angina. Coronary vasospasm tends to occur in focal areas in the coronary tree and can be readily induced by the use of various agents. Spontaneous severe multivessel spasm, mimicking severe obstructive coronary artery disease, has been infrequently described. The therapeutic dilemma in such a clinical situation is highlighted in our current case where an unnecessary coronary artery bypass graft surgery (CABG) was performed due to the lack of clinical suspicion of spasm. This patient presented 5 years after triple-vessel CABG with an episode of rest angina, and was initially found to have severe obstruction of all three native coronary arteries with patent grafts to the right coronary and left anterior descending arteries. After nitroglycerin injection, all three native vessels appeared large and normal. This report raises the question of whether the routine use of intracoronary nitroglycerin, largely abandoned over the past 20 years, should be revisited, at least for certain patient populations such as those with rest angina.     

Elevation of C-reactive protein in "active" coronary artery disease

Unstable angina occurs most commonly in the setting of atherosclerotic coronary artery disease (CAD), but there is little information concerning the mechanisms responsible for the transition from clinically stable to unstable coronary atherosclerotic plaque. Recently, increased focal infiltration of inflammatory cells into the adventitia of coronary arteries of patients dying suddenly from CAD and activation of circulating neutrophils in patients with unstable angina have been observed. To characterize the presence of inflammation in "active" atherosclerotic lesions, the acute phase reactant C-reactive protein (CRP) was measured in 37 patients admitted to the coronary care unit with unstable angina, 30 patients admitted to the coronary care unit with nonischemic illnesses and 32 patients with stable CAD. CRP levels were significantly elevated (normal less than 0.6 mg/dl) in 90% of the unstable angina group compared to 20% of the coronary care unit group and 13% of the stable angina group. The average CRP values were significantly different (p = 0.001) for the unstable angina group (2.2 +/- 2.9 mg/dl) compared to the coronary care (0.9 +/- 0.7 mg/dl) and stable angina (0.7 +/- 0.2 mg/dl) groups. There was a trend for unstable angina patients with ischemic ST-T-wave abnormalities to have higher CRP values (2.6 +/- 3.4) than those without electrocardiographic changes (1.3 +/- 0.9, p = 0.1). The data demonstrate increased levels of an acute phase reactant in unstable angina. These findings suggest that an inflammatory component in "active" angina may contribute to the susceptibility of these patients to vasospasm and thrombosis.     

Coronary hemodynamics in vasospastic angina: quantitative analysis by digital subtraction angiography

To evaluate the coronary circulation and myocardial perfusion dynamics, we performed left coronary digital subtraction angiography (DSA) in 35 patients with vasospastic angina. The left coronary circulation time (CCT) measured from the proximal left coronary artery to the coronary sinus was 5.77 +/- 0.86 sec, and the left epicardial conducting artery transmission time (CAT) measured from the proximal left coronary artery to the apical area was 2.65 +/- 0.82 sec in normal controls. The CCT and CAT were significantly prolonged in patients with vasospastic angina, indicating that the coronary peripheral vascular resistance is probably greater after the cessation of nitrates and Ca(++)-antagonists. After the intracoronary injection of ergonovine malate, the CCT was slightly shortened, but the apical T1/2 was significantly prolonged in patients with vasospastic angina. This suggested that coronary vasospasm is present not only in the epicardial arteries but also in coronary arteries with peripheral resistance. These phenomena were not observed in normal controls. We performed left coronary DSA after conventional left coronary cineangiography. When the CCT exceeded 6.7 sec, we considered that the coronary circulation was significantly impaired. We concluded that the coronary DSA is very useful for evaluating abnormal coronary circulation in patients with vasospastic angina during myocardial perfusion.     

Assessment of plexectomy in the treatment of severe coronary spasm in patients with normal coronary arteries

Surgical denervation of the heart by plexectomy was performed in 3 patients with variant angina, documented coronary spasm, and normal findings on coronary angiography. In all cases, spasm had already been responsible, preoperatively, for myocardial infarction and recurred thereafter in another territory despite medical therapy with a combination of nitrates and calcium antagonists. Plexectomy was performed using a standardized technique. The effectiveness of surgical suppression of cardiac autonomic innervation was confirmed postoperatively by pharmacologic tests. In 2 patients inferior myocardial infarction developed in the early postoperative period; in the third patient, coronary spasm recurred 3 weeks after plexectomy. Thus plexectomy, despite an adequate suppression of autonomic innervation, was ineffective in all cases and may even have been harmful in 2 patients. These data contradict the good results obtained by plexectomy associated with aortocoronary bypass in patients with variant angina and fixed stenotic coronary arteries. This discrepancy may be accounted for by a different pathophysiologic mechanism of vasospasm in normal coronary arteries and in diseased arteries at the site of the atheromatous stenosis. Thus, plexectomy should not be considered in the treatment of vasospasm involving normal coronary arteries, even if medical therapy fails to achieve satisfactory control of variant anginal attacks.     

Evaluation of coronary flow reserve in patients with vasospastic angina

OBJECTIVES: The presence of microvascluar impairment was evaluated in 154 patients with vasospastic angina identified by the acetylcholine provocation test. METHODS: Coronary flow reserve was evaluated with a Doppler flow guidewire in 128 vessels of 72 patients with chest pain, but no significant coronary stenosis(less than 50% stenosis) and no clinical factors that affect coronary flow reserve. Coronary flow reserve was obtained from the ratio of adenosine triphosphate-induced maximum/baseline averaged peak velocity. These vessels were classified into 2 categories according to whether acetylcholine-induced vasospasm was positive or negative. Vasospasm positive was defined as more than 90% stenosis provoked with chest pain and/or ischemic ST change. Positive vessels were subdivided according to focal or diffuse vasospasm. These vessels were also classified into 2 other categories according to whether vasospasm in the distal artery was positive or negative. RESULTS: Coronary flow reserve was significantly lower in vessels with vasospasm than in vessels without vasospasm in patients without vasospasm(2.9 +/- 0.8 vs 3.6 +/- 1.0, p = 0.0005). Coronary flow reserve was significantly lower in vessels without vasospasm in patients with vasospasm than in vessels without vasospasm in patients without vasospasm(3.0 +/- 0.8 vs 3.6 +/- 1.0, p = 0.03). There was no significant difference in coronary flow reserve between vessels with vasospasm and vessels without vasospasm in patients with vasospasm(2.9 +/- 0.8 vs 3.0 +/- 0.8, p = 0.8). There was no significant difference in coronary flow reserve between focal and diffuse vasospasm(3.2 +/- 0.8 vs 2.9 +/- 0.8, p = 0.3). Coronary flow reserve was significantly lower in vessels with vasospasm in the distal artery than in vessels without vasospasm in the distal artery (2.8 +/- 0.8 vs 3.4 +/- 1.0, p = 0.004). CONCLUSIONS: Patients with vasospastic angina have microvascular impairment in both vessels with vasospasm, and vessels without vasospasm. Microvascular impairment is prominent in vessels with vasospasm in the distal artery.     

Coronary flow reserve in patients with vasospastic angina: correlation between coronary flow reserve and age or duration of angina

OBJECTIVES: This study sought to assess the coronary flow reserve (CFR) in patients with pure vasospastic angina (VSA). METHODS AND RESULTS: The phasic flow velocities of both spasm-positive and spasm-negative coronary arteries of the left anterior descending artery (LAD) were recorded at rest and during hyperaemia (50 microg of adenosine triphosphate infusion intracoronary) using a 0.014 inch, 15 MHz Doppler guide wire in 42 patients with pure VSA and acetylcholine (ACh)-induced coronary artery spasms (20-100 microg), and 23 controls with normal coronary arteries without ACh-induced vasospasm. These 42 patients had 16 vessels with focal spasms (>99%), 17 vessels with diffuse spasms (>90%) in the LAD, and nine vessels with ACh-induced spasms in the right coronary artery, but not the LAD. Coronary flow reserve was obtained from the ratio of the hyperaemic/baseline time-averaged peak velocity. Coronary flow reserve did not differ between patients with VSA and the controls (2.9+/-0.8 versus 3.2+/-0.7, NS). Moreover, CFR did not differ among the four cases (focal: 2.8+/-0.7; diffuse: 3.0+/-0.9; non spasm: 2.9+/-0.7 versus controls: 3.2+/-0.7, respectively, NS). Coronary flow reserve in vessels with proximal spasms was significantly higher than that in vessels with mid or distal spasms (3.4+/-0.8 versus 2.6+/-0.6, 2.6+/-0.9, p<0.05). The only significant correlation was between CFR and age (p=0.0275) or the duration of angina before admission (p=0.0405). CONCLUSIONS: There was no difference in CFR in patients with ACh-induced spasms between the spasm-positive and spasm-negative vessels. Moreover, CFR was maintained normally in vessels with diffuse spasms, as in those with focal spasms. The most important determinant factors for CFR in patients with VSA were age and the duration of angina before admission.     

Myocardial ischemia due to vasospasm of small coronary arteries detected by methylergometrine maleate stress myocardial scintigraphy

BACKGROUND: Recently, several case reports have implicated vasospasm of small coronary arteries in vasospastic angina pectoris. Vasospasm of small coronary arteries was also considered from angiographic findings in patients with atypical chest pain. In Syrian hamster, vasospasm in small coronary arteries was considered to be the cause of dilated cardiomyopathy. HYPOTHESIS: This study was undertaken to determine whether vasospasm in small coronary arteries can be induced by methylergometrine maleate stress thallium-201 (201Tl) myocardial scintigraphy. METHODS: Twenty-five patients with chest pain, all of whom had intact coronary arteries, were studied. After intracoronary methylergometrine maleate injection, coronary arteriograms also looked normal in all cases. Thallium-201 myocardial scintigraphy was carried out immediately after intracoronary methylergometrine maleate injection in four patients with chest pain. In the remaining 21 patients with chest pain, methylergometrine maleate was given intravenously within up to 2 weeks before 201Tl myocardial scintigraphy. RESULTS: In the intracoronary injection study, one patient had chest discomfort after methylergometrine maleate injection, and ST-segment elevation was observed on electrocardiogram (ECG). Of the 21 patients with chest pain, 11 patients felt angina-like chest pain after intravenous injection of methylergometrine maleate, but their ECGs showed no ischemic changes. Stress 201Tl myocardial scintigrams showed methylergometrine maleate-induced perfusion defects with complete redistribution in 3 of 4 patients in the intracoronary injection study and in 12 of 21 patients in the intravenous injection study. These findings suggest that vasospasm in small coronary arteries caused myocardial ischemia in 15 of 25 patients (60%) with chest pain. CONCLUSION: Vasospasm in small coronary arteries may be involved in the myocardial ischemia of some patients with chest pain who do not show any large coronary artery vasospasm.     

Spontaneous alterations in coronary blood flow velocity before and after coronary angioplasty in patients with severe angina

Cyclic coronary artery flow variations with a spontaneous decline in coronary blood flow to very low levels have been documented in stenosed canine coronary arteries with endothelial injury. These flow variations are associated with transient platelet aggregation and dislodgment and the release of selected mediators, including thromboxane A2 and serotonin. However, cyclic or spontaneous flow variations have not been demonstrated in stenosed coronary arteries in humans. In this study, the hypothesis was tested that spontaneous coronary blood flow velocity variations occur in some patients with stenosed coronary arteries before or after coronary artery angioplasty. Thus, 13 patients with severe and limiting angina underwent intracoronary pulsed Doppler velocimetry of their dilated artery immediately before and after percutaneous transluminal coronary angioplasty, whereas 9 control patients underwent velocimetry of an angiographically normal coronary artery. A 3F catheter with a 20 MHz Doppler crystal was positioned to achieve a maximal stable signal, and the flow velocity signal was recorded continuously for 20 min. Spontaneous flow velocity variations (greater than or equal to 38% change in Doppler frequency shift with wide morphologic changes) were present in 3 of the 13 patients tested. Spontaneous flow velocity variations occurred before angioplasty in one patient, after angioplasty in another and both before and after angioplasty in a third. In addition, 2 of the 13 patients, 1 with spontaneous coronary artery flow velocity variations before angioplasty, had frank vasospasm in an adjacent area just distal to the area of coronary dilation immediately after balloon inflation. These data establish that spontaneous coronary artery flow velocity variations occur in some patients with severe and limiting angina before and after coronary angioplasty. These variations may be related to platelet aggregation or coronary vasoconstriction, or both, at sites of endothelial injury resulting from plaque fissuring or ulceration and endothelial and medial injury occurring during coronary angioplasty.     

Plaque morphology at coronary sites with focal spasm in variant angina: study using intravascular ultrasound.

In the present study, the intravascular ultrasound (IVUS) morphologic appearance of coronary atherosclerotic plaque associated with focal spasm was prospectively studied in 45 patients with or without focal coronary spasm provoked by ergonovine or acetylcholine. The percent plaque area and plaque arc were determined from the IVUS images at the sites of spasm. Calcified lesion was defined as the presence of high-intensity echo with acoustic shadowing. Twenty-three patients had focal coronary spasm defined as angiographic narrowing >75% and IVUS demonstrated atherosclerotic plaque in these 23 sites. In the 22 patients without focal spasm, IVUS demonstrated 18 atherosclerotic lesions in 17 patients and the remaining 5 patients did not have significant lesions. There was no difference in the percent plaque area and plaque arc between plaque lesions with (47+/-10%, 298+/-71 degrees ) and without (39+/-15%, 249+/-83 degrees ) coronary spasm. Interestingly, calcified lesion was less frequently present at the sites with than at those without spasm (p<0.05). These results indicate that the presence of plaque without calcification is likely to be related to the occurrence of focal vasospasm, although the severity and distribution of the disease did not differ between each patient group.     

The site of plaque rupture in native coronary arteries: a three-vessel intravascular ultrasound analysis

OBJECTIVES: We evaluated the axial location of plaque ruptures in native coronary arteries. BACKGROUND: It is clinically important to understand the potential sites of plaque rupture. METHODS: We performed three-vessel intravascular ultrasound (IVUS) examination in 392 patients; 231 had acute coronary syndrome (ACS) and 161 had stable angina pectoris (SAP). The IVUS detected plaque ruptures in 206 patients: 158 ACS patients and 48 SAP patients. The distance between each coronary plaque rupture segment and the respective coronary ostium was measured with motorized IVUS transducer pullback in all three coronary arteries. RESULTS: There were a total of 273 plaque ruptures in these 206 patients; 143 in the left anterior descending artery (LAD), 40 in the left circumflex artery (LCX), and 90 in the right coronary artery (RCA). There were 67 plaque ruptures in SAP patients and 206 in ACS patients; there were 197 culprit/target lesion plaque ruptures and 76 non-culprit/non-target lesion plaque ruptures. The LAD plaque ruptures were predominantly located between 10 and 40 mm from the LAD ostium (83%, 119 of 143). The LCX plaque ruptures were evenly distributed in the entire LCX tree. Most RCA plaque ruptures were located in segments between 10 and 40 mm (48%, 43 of 90) and in segments >70 mm from the ostium (32%, 29 of 90). CONCLUSIONS: Three-vessel IVUS imaging showed that plaque ruptures occurred mainly in proximal segments of the LAD (83% of LAD plaque rupture), the proximal and distal segments of the RCA (48% and 32% of RCA plaque ruptures, respectively), and the entire LCX.     

Spontaneous coronary artery spasm in variant angina is caused by a local hyperreactivity to a generalized constrictor stimulus

To assess whether spontaneous coronary artery spasm in patients with variant angina results from local coronary hyperreactivity to a generalized constrictor stimulus or from a stimulus generated only at the site of the hyperreactive segment, the behavior of spastic and nonspastic coronary segments was studied in six patients with variant angina in whom focal coronary spasm developed spontaneously during cardiac catheterization. None of the patients had critical (greater than 50% luminal diameter reduction) organic coronary stenoses. Coronary diameters were measured by computerized quantitative arteriography during control, spontaneous spasm and ergonovine-induced spasm and after intracoronary nitrates were given. During spontaneous spasm, the luminal diameter of spastic and both proximal and distal nonspastic coronary segments was significantly reduced from control values, 64.2%, 13.2% and 14.8%, respectively. Average diameter reduction of unrelated arteries was 12.3%. Ergonovine, which was also administered to four patients, provoked focal spasm at the same site as spontaneous spasm. During intravenous ergonovine, luminal diameter of spastic segments was reduced by 91.5%, that of nonspastic proximal segments by 17.8% and that of nonspastic distal segments by 11.5%. Luminal diameter of unrelated arteries during ergonovine-induced spasm was reduced by 17.7%. Constriction of spastic segments was greater during ergonovine-induced spasm (p less than 0.05), whereas the extent of diameter reduction of nonspastic segments was not significantly different during spontaneous spasm and ergonovine-induced spasm. Intracoronary isosorbide dinitrate dilated spastic and nonspastic coronary segments to a similar extent from control (20.7%, 18% and 16.5%, respectively; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Plaque ruptures in stable angina pectoris compared with acute coronary syndrome

BackgroundPlaque rupture is more frequently observed in patients with acute coronary syndrome (ACS) rather than in patients with stable angina pectoris (SAP). Consequently, studies regarding plaque rupture, which occurred in SAP patients, are rare. Therefore, we evaluated the frequency and axial location of plaque ruptures in SAP patients and compared them with those in ACS patients.MethodsThree hundred ninety-two patients (231 ACS and 161 SAP patients) who were scheduled for coronary intervention underwent three-vessel intravascular ultrasound (IVUS) study. IVUS criteria for plaque rupture were a plaque contained a cavity that communicated with the lumen with an overlying residual fibrous cap fragment. Using motorized IVUS transducer pullback in all three coronary arteries, the distance between each coronary plaque rupture segment and the respective coronary ostium was measured.ResultsPlaque ruptures were detected in 206 of 392 patients who underwent three-vessel intravascular ultrasound examination. At least one plaque rupture in any coronary artery was noted in 48 (30%) SAP and 158 (68%) ACS patients (p < 0.001). In both ACS and SAP patients, plaque ruptures were clustered mainly in the proximal segments of the left anterior descending artery and in the proximal and distal segments of the right coronary artery.ConclusionsAt least one plaque rupture in any coronary artery was noted in 30% of SAP patients. Like in ACS patients, plaque ruptures were clustered mainly in the proximal segments of the left anterior descending artery and in the proximal and distal segments of the right coronary artery in SAP patients.     

Cardiac events in vasospastic angina: site and morphology of coronary artery spasm is related to the long-term prognosis of vasospastic angina

To determine whether the site and morphology of coronary artery spasm provoked with acetylcholine can predict the long-term prognosis of vasospastic angina, coronary artery spasm (more than 90% narrowing) provoked with acetylcholine was studied in 66 consecutive patients (56 males, 10 females, mean age 56 +/- 9 years) with vasospastic angina. All patients were followed for 6.7 +/- 0.9 years and the incidence of cardiac events such as sudden death, myocardial infarction or worsened unstable angina was compared with the site and morphology of provoked spasm. The site of spasm was regarded as proximal when spasm occurred in the proximal site of 3 major coronary arteries which was designated as segment 1, 6 or 11, according to the classification of the American Heart Association, and distal in other segments. The morphology of spasm was classified into 3 types, focal (12 cases, localized more than 90% narrowing with adjoining parts constricting less than 25%), diffuse (17 cases, diffuse more than 90% narrowing), and intermediate (37 cases, localized more than 90% narrowing with adjoining parts constricting 25-90%). The site of spasm was classified into 2 types, the proximal group (24 cases) and the distal group (42 cases). Cardiac events occurred in 7 patients during the follow-up period: sudden death in 2, myocardial infarction in 2, and worsened unstable angina in 3. As to the site of spasm, the incidence of cardiac events was 21% (5/24 patients) in the proximal group, significantly higher than 5% (2/42) in the distal group (p < 0.05). As to the site of spasm, the incidence of cardiac events was 41% (5/12) in the focal group, significantly higher than 3% (1/37) in the intermediate group and 6% (1/17) in the diffuse group (p < 0.001). The presence of proximal and focal coronary artery spasm was associated with a significantly higher incidence of cardiac events. The site and morphology of coronary artery spasm provoked with acetylcholine is related to the long-term prognosis of vasospastic angina.     

Possible contribution of C-reactive protein within coronary plaque to increasing its own plasma levels across coronary circulation

C-reactive protein (CRP) mRNA was detected in coronary plaque. Plasma CRP levels across the coronary circulation were increased much more in patients with unstable angina pectoris and somewhat more in those with stable angina pectoris compared with controls whose coronary arteries were angiographically normal. Thus, CRP within coronary plaque might contribute to increased plasma CRP levels across coronary circulation, particularly among patients with unstable angina pectoris.     

The heart in fatal unstable angina pectoris

Compared to patients with sudden coronary death and acute myocardial infarction, relatively little morphologic data has been reported in patients with unstable angina pectoris. This article reviews necropsy data collected from one laboratory on unstable angina pectoris. From these data, several observations are appropriate: (1) Patients with unstable angina as a group have more coronary narrowing by atherosclerotic plaque than do patients with sudden coronary death or acute or healed myocardial infarction. (2) Patients with unstable angina have a much higher frequency of severe narrowing of the left main coronary artery than do patients in other coronary subsets. (3) The coronary atherosclerotic plaques in unstable angina consist primarily of fibrous tissue, and they are more similar to those found in patients with sudden coronary death than in patients with acute myocardial infarction. (4) The frequency of acute coronary lesions (thrombi, plaque rupture, and plaque hemorrhage) is similar to that observed in patients with sudden coronary death and significantly less than that observed in acute myocardial infarction. (5) The frequency of multiluminal channels throughout the major coronary arteries is significantly higher in unstable angina compared to sudden coronary death or acute myocardial infarction. (6) The major epicardial arteries and the heart are smaller in patients with unstable angina than in patients with sudden coronary death or acute myocardial infarction. (7) The left ventricular cavity is usually of normal size in patients with unstable angina and therefore left ventricular function is usually normal.     

Intravascular ultrasound findings of negative arterial remodeling at sites of focal coronary spasm in patients with vasospastic angina

BACKGROUND: There are few data about the intravascular ultrasound (IVUS) findings in patients with vasospastic angina, especially regarding patterns of vascular remodeling. METHODS AND RESULTS: Coronary spasm was documented by angiography and electrocardiographic evidence of ischemia in 36 patients after administration of ergonovine (cumulative doses up to 350 microg). After relief of spasm with 1000 microg of intracoronary nitroglycerin, quantitative angiography and IVUS imaging were performed and analyzed by standard methods. The 36 focal spasm sites were compared with the proximal and distal reference segments. The angiographic baseline minimum lumen diameter measured 1.78 +/- 0.66 mm, which decreased to 0.66 +/- 0.38 mm with ergonovine provocation (P <.0001), increased to 2.66 +/- 0.64 mm after intracoronary nitroglycerin (P <.0001 compared with baseline and after ergonovine), and did not change after IVUS imaging (2.66 +/- 0.63, P =.9). By IVUS, atherosclerotic lesions were observed at all coronary spasm sites; the mean plaque burden measured 56% at the spasm site and 35% at the reference. Spasm site plaque composition was hypoechoic in 31 and hyperechoic, noncalcific in 5; there was no calcium. The mean eccentricity index (maximum divided by minimum plaque thickness) was 6.7. Positive remodeling (spasm site arterial area greater than proximal reference) was present in 5; intermediate remodeling (proximal reference greater than spasm site greater than distal reference arterial area) was present in 7; and negative remodeling (spasm site arterial area less than distal reference) was present in 24. CONCLUSIONS: Sites of vasospasm in patients with variant angina showed characteristics of early atherosclerosis, except for an unusually high incidence of negative arterial remodeling.