Comparison of serum levels of inflammatory markers in patients with coronary vasospasm without significant fixed coronary artery disease versus patients with stable angina pectoris and acute coronary syndromes with significant fixed coronary artery disease

Serum levels of inflammatory markers (interleukin-6, monocyte chemoattractant protein-1, soluble intercellular adhesion molecule-1, soluble vascular adhesion molecule-1, and C-reactive protein) were measured at baseline in serum samples from 189 patients who were admitted for coronary angiography because of suspected ischemic heart disease. Median duration of follow-up was 28 months. Patients in our sample were enrolled in 4 diagnostic groups: no hemodynamically significant coronary artery disease (CAD) and no coronary vasospasm (control group, n = 32), hemodynamically significant CAD and stable angina pectoris (SAP group, n = 34), coronary vasospastic angina pectoris without hemodynamically significant CAD (vasospasm group, n = 31), and acute coronary syndrome (ACS) and hemodynamically significant CAD (ACS group, n = 92). Overall, the level of serum inflammatory markers was highest in the ACS group and lowest in the control group, with intermediate values observed in the SAP and vasospasm groups, with the exception of soluble intercellular adhesion molecule-1, the level of which was highest in the vasospasm group. Multivariate analysis showed that log (interleukin-6) was independently associated with a diagnosis of coronary vasospastic angina pectoris in patients without hemodynamically significant CAD (odds ratio 8.48, p = 0.027). Patients in the ACS group had a significantly lower survival rate compared with the other 3 groups but without an independent predictor that could be identified in this patient cohort. Recurrent angina pectoris occurred with similar rates in the SAP, vasospasm, and ACS groups. The independent predictor for recurrent angina pectoris was treatment that did not include clopidogrel (odds ratio 3.88, p = 0.007). In conclusion, the results of this study suggest that inflammation can exist in coronary vasospasm without hemodynamically significant CAD.     

Comparison of clinical characteristics and prognosis in Taiwanese patients with coronary vasospastic angina pectoris without significant fixed coronary artery disease versus patients with significant fixed coronary artery disease and either stable angina pectoris or acute coronary syndromes

BACKGROUND: Limited information is available comparing the clinical characteristics and prognosis for patients with coronary vasospastic angina in the absence of hemodynamically significant coronary artery disease (CAD) (defined as >50% stenosis) versus patients with significant fixed CAD presenting with either stable angina pectoris (SAP) or acute coronary syndromes (ACS). METHODS: Patients who underwent cardiac catheterization for suspected ischemic heart disease between August 1999 and February 2003 were followed clinically. For patients without hemodynamically significant CAD, a provocation test for coronary vasospasm was undertaken using a step-wise dose of intracoronary ergonovine administration. RESULTS: A total of 1134 patients were enrolled in the final analysis and stratified into 4 diagnostically distinct groups: control group (n = 239; mild CAD without coronary vasospasm); vasospasm group (n = 284; coronary vasospastic angina pectoris without hemodynamically significant CAD); SAP group (n = 110; hemodynamically significant CAD with SAP); ACS group (n = 501; hemodynamically significant CAD with ACS). Comparison of these 4 groups revealed that the ACS patients were more likely to be male, current smokers, and have hypercholesterolemia. In addition, this group had a significantly higher incidence of typical angina pectoris, 3-vessel CAD, and lower left ventricular ejection fraction. Between-group comparison revealed that vasospasm patients had a significantly higher incidence of early morning angina pectoris. Multivariate analysis showed that current smoking was the most independent risk factor associated with the diagnosis of coronary vasospastic angina pectoris in patients without hemodynamically significant CAD. During a median follow-up period of 49 months, recurrent angina pectoris was noted in patients from the control (n = 6; 3%), SAP (n = 9; 8%), vasospasm (n = 30, 11%), and ACS groups (n = 92; 18%); with nonfatal myocardial infarction identified during follow-up in the SAP (n = 5; 5%), vasospasm (n = 3; 1%), and ACS groups (n = 37; 7%). In addition, 29 and 3 cardiac deaths occurred in the ACS and SAP groups, respectively, whereas there were no such mortalities in the control and vasospasm groups. CONCLUSIONS: Early morning angina pectoris and cigarette smoking were the most common clinical characteristics in patients with coronary vasospasm. These patients had an excellent prognosis despite the possibility of recurrences of vasospastic angina pectoris.     

Comparison of epicardial coronary artery tone and reactivity in Prinzmetal's variant angina and chronic stable angina pectoris

It has been suggested that a generalized coronary vasomotion disorder is present in variant angina and that evaluation of baseline coronary artery tone may be useful for predicting the occurrence of coronary artery spasm. The vasomotor response of angiographically normal proximal and distal coronary artery segments was studied in 9 patients with atypical chest pain and normal coronary arteriograms (control group), 13 patients with active variant angina and 41 patients with chronic stable angina. Ergonovine (intravenous, 100 to 300 micrograms, or intracoronary, 8 to 20 micrograms, was administered to all 22 patients in the control and variant angina groups and to 11 of the 41 patients with chronic stable angina. All patients also received intracoronary isosorbide dinitrate (1 to 2 mg). Computerized coronary artery diameter measurement of angiographically normal segments was carried out before and after ergonovine and nitrate administration. Mean baseline intraluminal diameter of proximal and distal coronary segments was not significantly different in control patients and those with variant angina (nonspastic segments only) or coronary artery disease (proximal 2.89 +/- 0.15, 2.83 +/- 0.14 and 2.82 +/- 0.09 mm; distal 1.60 +/- 0.08, 1.63 +/- 0.07 and 1.62 +/- 0.06 mm, respectively). After ergonovine, proximal segments constricted by 10 +/- 2%, 15 +/- 3% and 11 +/- 4% and distal segments by 11 +/- 3%, 11 +/- 2% and 14 +/- 3% in control, variant angina and coronary artery disease groups, respectively (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Breathlessness, angina pectoris and coronary artery disease

The relation of breathlessness to angina was examined in 7,735 middle-aged British men. Among men who did not report breathlessness, the age-standardized prevalence rate of angina was 4%. In men with mild, moderate or severe breathlessness, the prevalence rates of angina were 16, 29 and 41%, respectively. The association between breathlessness and angina was independent of age or cigarette smoking, with similar relations observed in men who had never smoked. The prevalence of electrocardiograms revealing ischemia increased with the severity of breathlessness, even in men without angina or other evidence of coronary artery disease (CAD) at screening. In men with a low forced expiratory volume in 1 second, the prevalence of angina was also increased, but the association was much weaker than that observed between angina and breathlessness. After a 5-year follow-up, 25% of men severely breathless at screening but without any initial evidence of CAD had developed angina, 5% had had a heart attack (half of these were fatal) and 7% were dead from causes other than CAD. The corresponding rates for men not breathless at screening and without evidence of CAD were: 4% angina, 2.5% heart attack and 2% dead from causes other than CAD. Breathlessness appears to be an early indicator of CAD in the absence of either angina or electrocardiographic evidence of ischemia.     

Dental pain threshold and angina pectoris in patients with coronary artery disease

One hundred eight consecutive patients with proved coronary artery disease and reproducible exercise-induced myocardial ischemia were studied. During repeated exercise testing, 52 patients (Group I) had myocardial ischemia in the absence of pain (silent ischemia) whereas 56 patients (Group II) experienced anginal symptoms in the presence of electrocardiographic signs of ischemia. A pulpal test was carried out in all patients using an electrical dental stimulator commonly used in dentistry. Electrical current was delivered in increasing intensity from 10 to 500 mA, and the dental pain threshold and the reaction of the patients to maximal stimulation were determined. During the pulpal test, 71.2% of the patients in Group I did not experience pain, even at maximal stimulation (threshold 0), 11.5% were sensitive at threshold I (10 to 200 mA) and 17.3% felt pain at threshold II (210 to 500 mA). In Group II, 69.7% of the patients complained of dental pain at the low intensity test current (threshold I), 10.7% at threshold II and 19.6% at threshold 0. In Group I, 71.2% of patients did not have discomfort (reaction -), even at maximal stimulation, 21.1% had a mild reaction (reaction +) and 7.7% had an intense painful reaction (reaction ++). In Group II, 80.4% of patients were sensitive to the pulpar test (67.9% reported intense painful sensation at maximal stimulation, 12.5% had a mild reaction); 19.6% of patients had no reaction. The two groups of patients were similar with respect to age, sex and angiographic features.(ABSTRACT TRUNCATED AT 250 WORDS)     

Three-vessel coronary artery spasm in a patient with variant angina and normal coronary arteries

Variant angina with two or more electrocardiographic or angiographic localizations has seldom been reported [1-4]. We present a case of variant angina pectoris and normal coronary arteries with three different and independent electrocardiographic localizations.     

Aortic stenosis,angina pectoris,coronary artery disease

The data from 88 patients (pts) with aortic stenosis (AS) were reviewed to determine relationships between angina pectoris (AP) and coronary artery disease (CAD). Results of surgery performed in 81 of these pts was analyzed. All pts had coronary arterlograms, and lesions ≥ 50% were considered significant. Fifty-nine pts had an aortic valve gradient measured at catheterization ≥ 40 mmHg, and in 29 pts, AS was confirmed at operation. Sixty-eight pts (77%) experienced AP, and 32 had coexisting CAD (47%); 9 of 20 pts without AP had CAD (45%). There were no significant differences in the incidence of AP in pts divided into subgroups by the aortic valve gradient (40–50, 51–100, 101–200 mmHg) or age (40–59, 60–81 years. Also, no significant differences were found in the incidence or extent of CAD between the two age groups; the extent of CAD was similar regardless of the presence or absence of AP. In pts with AP (1) CAD was more likely in pts ≥ 60 years of age; (2) CAD was less likely when the aortic valve gradient was > 100 mmHg, suggesting that AP in these pts was due to hemodynamically severe AS. All pts with 3-vessel CAD experienced AP, and the aortic valve gradient was less in these pts than in those with no CAD or less extensive CAD. In 19 pts with combined AS and CAD who had both the aortic valve replaced and a revascularization operation only 1 of pts died in the hospital, while 3 of 19 pts with combined AS and CAD who had aortic valve replacement alone died. In this study a significant number of pts with AS experienced AP, and the presence or absence of AP did not predict coexisting CAD. Coronary arteriography is recommended in the evaluation of pts ≥ 40 years of age with AS. The operative mortality appears to be decreased in pts with AS and CAD who have combined surgery.     

Distribution and severity of coronary artery disease in 500 patients with angina pectoris

The distribution and severity of coronary disease in 500 patients with angina pectoris and at least one area of 50% or greater reduction of luminal diameter in a major coronary artery were compared with respect to patients' age and coronary arterial pattern. The coronary arterial patterns were separated into right (360 patients), mixed (89 patients), and left (51 patients) systems, depending upon the blood supply to the inferior surface of the left ventricle. The following relationships were noted: 1) In patients with angina pectoris, the distribution and severity of coronary artery disease is similar from the third to eighth decade. 2) Coronary arterial stenoses of 50-70% of greater reduction of luminal diameter involve most frequently the proximal portion of the major vessels. Coronary artery disease is multivessel in nature in 80% of cases. In single vessel disease the left anterior descending artery is involved most frequently. 3) The left main coronary artery is moderately to severely obstructed less frequently in individuals with left (2%) as compared to right (8%) and mixed (10%) systems. Otherwise, the distribution of coronary artery disease is similar in right, mixed, and left systems. 4) Coronary artery disease is a diffuse rather than a focal process. As demonstrated by coronary arteriography, patients with coronary artery disease have smaller vessels throughout the arterial tree as compared with individuals free of evident coronary atherosclerosis.     

Oesophageal function in patients with angina pectoris: a comparison of patients with normal coronary angiograms and patients with coronary artery disease

Oesophageal function was assessed in 52 patients with angina pectoris whose coronary angiograms were completely normal and in 21 patients with angina pectoris who had significant coronary artery disease. During a standard oesophageal manometric study, abnormalities were found in 23 (44%) patients with normal coronary angiograms but in only 2 (10%) patients with coronary artery disease (p less than 0.01). Twenty-four (46%) patients with normal coronary angiograms were found to have gastro-oesophageal reflux disease during 24-hour oesophageal pH monitoring. Of the 52 patients with normal coronary angiograms, 19 (37%) had gastro-oesophageal reflux disease and abnormal oesophageal motility, 5 (10%) had gastro-oesophageal reflux disease alone, and 7 (13%) had oesophageal motility disorder alone. The use of provocation procedures, including intravenous edrophonium during oesophageal manometry and treadmill exercise testing during pH monitoring, enabled the oesophageal abnormality to be demonstrated simultaneously with chest pain in 25 of these 31 patients. Typical angina pectoris, coincident with abnormal oesophageal motility, was precipitated in a subgroup of patients who had been shown to have oesophageal manometric abnormalities and gastro-oesophageal reflux disease by the infusion of hydrochloric acid into the oesophagus; both the chest pain and manometric abnormality resolved following the oral administration of antacid.     

Pacing-induced angina pectoris and induction of ventricular arrhythmias in coronary artery disease

Ischemia caused by rapid pacing during electrophysiologic study could facilitate induction of ventricular arrhythmias. The results of extrastimulation were retrospectively analyzed in 32 patients with coronary artery disease (CAD) without a history of symptomatic arrhythmia. These patients were studied at cardiac catheterization for angina pectoris refractory to medical therapy. Eleven patients (group I) had typical angina during trains of rapid right ventricular pacing (repeated trains of 8 stimuli [mean cycle length (CL) 473 +/- 47 ms]) but were asymptomatic during slower trains (CL 800 +/- 100 ms). Twenty-one patients (group II) had no symptoms with either rapid (CL 448 +/- 51 ms) or slow (CL 688 +/- 105 ms) trains, despite comparable left ventricular function, CAD severity and medication. Effective refractory periods (S1S2) after rapid drive were shorter in group I than in group II patients (225 +/- 9 vs 240 +/- 14 ms, p less than 0.002), but refractory periods during slow pacing were similar (251 +/- 12 vs 253 +/- 17 ms, difference not significant). No patient in either group had sustained arrhythmia (more than 15 beats) induced by single and double ventricular extrastimuli, decrementally applied at the right ventricular apex. The number of extra beats provoked in group I when rapid trains caused angina (4.3 +/- 3.6) was similar to that induced by extra-stimulation after slower pacing without angina (4.4 +/- 3.5) and to that obtained with rapid or slow pacing in group II (3.1 +/- 3.3 and 2.8 +/- 2.2).(ABSTRACT TRUNCATED AT 250 WORDS)     

Nocturnal angina: precipitating factors in patients with coronary artery disease and those with variant angina

Factors precipitating nocturnal myocardial ischaemia were investigated in 10 patients with frequent daytime and nocturnal angina pectoris. Eight patients had fixed obstructive coronary artery disease or a low exercise threshold or both before the onset of ischaemia. Two patients had variant angina with normal coronary arteries and negative exercise tests. During sleep the electrocardiogram, electroencephalogram, electro-oculogram, electromyogram, chest wall movements, nasal airflow, and oxygen saturation were continuously measured. Forty two episodes of transient ST segment depression were recorded in the eight patients with coronary artery disease and 26 episodes of ST segment depression and elevation in the two patients with variant angina and normal coronary arteries. All episodes of ST segment depression in the former group of patients were preceded by an increase in heart rate as a result of arousal and lightening of sleep, bodily movements, rapid eye movement sleep, or sleep apnoea (one episode). In contrast, in the variant angina group no increase in heart rate, arousal, or apnoea preceded 23 of the 26 episodes of ST segment change. Thus increase in myocardial oxygen demand was important in precipitating nocturnal angina in patients with coronary artery disease and reduced coronary reserve. In the patients with coronary spasm these factors did not often precede the onset of nocturnal myocardial ischaemia.     

Aortic stenosis, angina pectoris, and coronary artery disease.

The relationships between aortic stenosis, coronary artery disease, angina pectoris, and myocardial infarction were examined in 173 patients with isolated calcific aortic stenosis who had coronary arteriography as well as cardiac catheterization. All were over age 40 and had definite cardiac symptoms; 156 later had aortic valve replacement. Coronary lesions narrowing the lumen by 50% or more were present in 37% of patients aged 40 to 59 and 68% of those aged 60 to 82. Coronary disease was present in 64% of patients with angina pectoris and 33% of those without angina. Angina which occurred only in association with dyspnea on exertion was associated with coronary disease in 45% of instances, whereas angina which also occurred on exertion without any dyspnea or which occurred with emotional stress, after meals, during sleep, or at rest unprovoked was associated with coronary disease in 80% of instances. Patients with coronary disease without any chest pain or with atypical pain considered nonanginal were men, usually over age 60, with congestive heart failure as the predominant symptom. Electrocardiograms showing transmural inferior or anterolateral infarction nearly always indicated coronary disease, while QS patterns in Leads V1-2 occurred frequently with normal coronary arteries. Serum cholesterol was elevated in 23% of those with coronary disease and 8% of those without. A group of patients with moderate aortic stenosis could be identified, with aortic valve areas of 0.55 to 0.80 cm. per square meter, in whom coronary disease was the sole or chief cause of symptoms. The operative mortality rate with aortic valve replacement was 9.6% in those with coronary disease and 1.4% in those without significant coronary disease. Coronary disease is frequently present in patients with calcific aortic stenosis, particularly in those over 60, those with angina, and those with symptoms despite only moderate aortic stenosis. The type of anginal syndrome, the ECG evidence of transmural infarction, and the coronary risk factors provide additional clues for clinical diagnosis.