Congenital graves disease. Four familial cases with long-term follow-up and perspective

In four patients with Prinzmetal's variant form of angina, the attack was induced by the combined administration of epinephrine (0.4 to 0.5 mg, given subcutaneously at 7:30 to 8:00 A.M.) and propranolol (40 mg. given orally at 5:00 A.M.). Selective coronary cinearteriography was done before, during, and after the attack with constant monitoring of the ECG and blood pressure. Severe spasm of the right coronary artery occurred at the proximal portion in association with ST-segment elevation in Lead III during the attack and disappeared with the subsidence of the attack in all of them. These results strongly suggest that severe spasm of a large coronary artery mediated by alpha-adrenergic receptors is responsible for the attack of Prinzmetal's variant form of angina.     

Clinical syndrome of variant angina with normal coronary arteriogram

We compared patients with variant angina (ST-segment elevation during pain) who had normal or near normal coronary arteriograms (Group 1) with 20 in whom variant angina occurred in the presence of obstructive coronary lesions (Group 2). A long history of nonexertional angina without angina of effort or previous infarction was the rule in Group 1, whereas recent-onset unstable angina preceded by effort angina and infarction predominated in Group 2 (P less than 0.001). Normal electrocardiograms at rest, with ischemic ST-segment elevation in the inferior leads, and ischemia-induced heart block and bradycardia, characterized Group 1, whereas abnormal electrocardiograms, ischemic involvement or fibrillation were more common in Group 2 (P less than 0.001). Variant angina with normal coronary arteriogram generally has a benign course and is probably unrelated to atherosclerosis.     

Unstable angina: are we able to recognize high-risk patients?

It is difficult to identify characteristics of patients with unstable angina that are predictive of a high likelihood of developing clinical events. However, several features have been recognized. Patients with a clinical history of previous stable exertional angina symptoms who began to experience rest pain appear to be at risk and tend to have more extensively underlying coronary disease. When the ischemic episodes are accompanied by rates, a new or worsening mitral regurgitation murmur, or hypotension, there is a high likelihood of significant coronary artery disease and one should triage these patients to early cardiac catheterization and prompt revascularization. An angiographic feature that carries a high risk is a lesion in the proximal left anterior descending or in the left main coronary artery. Certain typical ECG patterns are very suggestive for a critical narrowing in these coronary arteries. If chest pain and ST-segment changes recur on vigorous medical management, early invasive evaluation should be strongly considered. Even so, the left ventricular function is very important prognostically. According to serologic tests, the level of C-reactive protein and serum amyloid A protein suggesting that there may be active inflammation predicts an early poor outcome. However, these serologic abnormalities do not have much clinical value. An increased platelet activation and a reduced fibrinolytic capacity play a role in the pathogenesis of unstable angina, but thrombolytic therapy does not improve the prognosis in patients with unstable angina.     

Angina pectoris caused by coronary microvascular spasm

BACKGROUND: Microvascular angina can occur during exercise and at rest. Reduced vasodilator capacity of the coronary microvessels is implicated as a cause of angina during exercise, but the mechanism of angina at rest is not known. Our aim was to test the hypothesis that primary hyperconstriction (spasm) of coronary microvessels causes myocardial ischaemia at rest. METHODS: Acetylcholine induces coronary artery spasm in patients with variant angina. We tested the effects of intracoronary acetylcholine at graded doses in 117 consecutive patients with chest pain (at rest, during exertion, or both) and no flow-limiting (>50%) organic stenosis in the large epicardial coronary arteries. We also assessed the metabolism of myocardial lactate during acetylcholine administration in 36 of the patients by measurement of lactate in paired blood samples from the coronary artery and coronary sinus vein. FINDINGS: Of the 117 patients, 63 (54%) had large-artery spasm, 29 (25%) had microvascular spasm, and 25 (21%) had atypical chest pain. The 29 patients with microvascular spasm developed angina-like chest pain, ischaemic electrocardiogram (ECG) changes, or both spontaneously (two patients) or after administration of acetylcholine (27 patients) without spasm of the large epicardial coronary arteries. Testing of paired samples of arterial and coronary sinus venous blood showed that lactate was produced during angina attack in nine of 11 patients with microvascular spasm. There was more women (p<0.01) and fewer coronary risk factors (p<0.01) in patients with microvascular spasm than in those with large-artery spasm. INTERPRETATION: Coronary microvascular spasm and resultant myocardial ischaemia may be the cause of chest pain in a subgroup of patients with microvascular angina.     

Production of a mouse/human chimeric IgE monoclonal antibody to the house dust mite allergen Der p 2 and its use for the absolute quantification of allergen-specific IgE

1. We evaluated the antianginal effects of YM430 in several experimental models in vitro and in vivo. 2. In isolated dog coronary artery, YM430 (10(-8)-10(-6) M) inhibited 3,4-diaminopyridine-induced rhythmic contractions with an IC50 value of 59.2 nM. 3. In anesthetized rats, YM430 (10-100 mg/kg PO) inhibited arginine vasopressin-induced ST-segment depression with an IC50 value of 36.6 mg/kg PO. 4. In anesthetized dogs, YM430 (0.3 mg/kg IV) significantly inhibited ST-segment elevation induced by coronary artery occlusion. 5. These findings suggest that YM430 may be of value in the treatment of various types of angina pectoris such as variant and stable angina.     

Heart rate variability in multiple sclerosis during a stable phase

BACKGROUND: Patients with ambulatory electrocardiographic (AECG) ST-segment depression and critical coronary narrowing are known to be at increased risk for adverse outcome, but little is known about patients with AECG ST-segment depression without critical coronary narrowing. HYPOTHESIS: The objectives of this study were to characterize the coronary angiographic pathology in patients with AECG ST-segment depression but without critical (< 50% diameter stenosis) coronary narrowing and to compare demographic and clinical findings in these patients with those enrolled in the Asymptomatic Cardiac Ischemia Pilot Study with AECG ST-segment depression and critical (> or = 50% diameter stenosis) coronary narrowing. METHODS: Coronary angiograms from patients with AECG ST-segment depression were reviewed in a central laboratory and quantitative measurement of percent stenosis was performed. Clinical and angiographic comparisons were made between patients with and without critical coronary narrowing. RESULTS: Patients without critical coronary narrowing (n = 64) were younger (p = 0.02), less likely to be male (p < 0.001) or to have risk factors for coronary atherosclerosis or a history of myocardial infarction (p < 0.001), and had fewer ischemic episodes per 24 h on the screening AECG (p = 0.02) than patients with critical coronary narrowing (n = 441). Of patients without critical narrowing, one half had angiographic evidence for coronary artery disease (> or = 20% stenosis) and 60% had an ejection fraction > 70%. CONCLUSIONS: Patients with AECG ST-segment depression without critical coronary narrowing are heterogeneous, with half having measurable coronary artery disease. Demographically and clinically, they appear to be different than patients with AECG ST-segment depression with critical coronary narrowing.     

A new noninvasive method of diagnosing vasospastic angina based on dilation response of the left main coronary artery to nitroglycerin as measured by echocardiography

OBJECTIVES: The purpose of the present study was to evaluate the feasibility of diagnosing vasospastic angina based on coronary artery tone as assessed by M-mode echocardiographic measurement of the dilation response of the left main coronary artery to nitroglycerin. BACKGROUND: The definite diagnosis of vasospastic angina is done by a coronary spasm provocative test using ergonovine maleate or acetylcholine during cardiac catheterization. Current noninvasive, nonpharmacologic diagnostic methods are not sensitive enough for the diagnosis of vasospastic angina. METHODS: Thirty-eight patients who had an angiographically normal left main trunk were studied. These patients were classified into four groups based on the presence or absence of more than 50% stenosis in the coronary arteries except for the left main trunk and the results of the acetylcholine or ergonovine provocative test. At 7 a.m. and at noon on the same day, the left main trunk diameter was measured by M-mode echocardiography before and after sublingual administration of nitroglycerin (0.3 mg), and its present dilation was calculated to assess coronary artery tone. RESULTS: The percent dilation of the left main trunk diameter induced by sublingual nitroglycerin at 7 a.m. and at noon was 22.4 +/- 4.7% (mean +/- SD) and 18.1 +/- 4.0% in 11 patients with vasospastic angina and without coronary stenosis, 14.9 +/- 7.1% and 11.2 +/- 6.9% in 9 patients with vasospastic angina and coronary stenosis, 6.1 +/- 3.5% and 7.0 +/- 5.1% in 8 patients without vasospastic angina but with coronary stenosis and 8.1 +/- 5.6% and 7.8 +/- 5.7% in 10 control subjects. The percent dilation at 7 a.m. was significantly greater in the vasospastic angina without coronary stenosis group than in the remaining three groups, and in the vasospastic angina groups, the percent dilation at 7 a.m. was significantly greater than that at noon. When percent dilation at 7 a.m. exceeding 15% was defined as positive for the diagnosis of vasospastic angina, the sensitivity was 80% and the specificity 94%. CONCLUSIONS: Basal tone of the left main trunk is elevated in the early morning in vasospastic angina. Dilation of the left main trunk diameter exceeding 15% induced by sublingual nitroglycerin in the early morning as measured by M-mode echocardiography is a highly sensitive and specific criterion for the diagnosis of vasospastic angina.     

Action of intracoronary nitroglycerin in refractory coronary artery spasm

Coronary artery spasm usually responds to sublingual nitroglycerin. This report describes four patients with variant angina and one patient with rest angina who had coronary spasm that was refractory to sublingual or i.v. nitroglycerin. In four patients, spasm occurred spontaneous and in one patient after 0.05 mg of ergonovine. In each case, 25-100 micrograms of intracoronary nitroglycerin promptly (30-45 seconds) resulted in reopacification of the vessel involved in spasm and resolution of evidence for ischemia. Thus, intracoronary nitroglycerin can reverse coronary artery spasm that does not respond to systemic nitroglycerin administration.     

Does acute improvement of endothelial dysfunction in coronary artery disease improve myocardial ischemia? A double-blind comparison of parenteral D- and L-arginine

OBJECTIVES: Parenteral L-arginine will improve myocardial ischemia in patients with obstructive coronary artery disease. BACKGROUND: Endothelial dysfunction causes coronary arterial constriction during stress, and L-arginine improves endothelial dysfunction. METHODS: Twenty-two patients with stable coronary artery disease and exercise-induced ST-segment depression underwent assessment of forearm endothelial function with acetylcholine and symptom-limited treadmill exercise testing during dextrose 5% infusion and after double-blind intravenous administration of L- and D-arginine (5 mg/kg/min) for 20 min. RESULTS: Forearm blood flow increased with both L- and D-arginine (33%+/-6% and 38%+/-7%, respectively, p < 0.001). Acetylcholine-mediated forearm vasodilation also improved with both L- and D-arginine (p < 0.0001). The magnitude of improvement was similar with both enantiomers and was observed in patients throughout the range of acetylcholine responses and cholesterol levels. Heart rate and blood pressure at rest and during each stage of exercise and exercise duration remained unchanged with L- and D-arginine compared to control. Ischemic threshold, measured either as the rate-pressure product or the duration of exercise at the onset of 1-mm ST-segment depression during exercise, also remained unchanged. Serum arginine, insulin and prolactin levels (p < 0.01) increased with both enantiomers. CONCLUSIONS: Parenteral arginine produces non-stereo-specific peripheral vasodilation and improves endothelium-dependent vasodilation in patients with stable coronary artery disease by stimulation of insulin-dependent nitric oxide release or by nonenzymatic nitric oxide generation. Despite enhanced endothelial function, there was no improvement in myocardial ischemia during stress with either enantiomer. Whether parenteral arginine will be of therapeutic benefit in acute coronary syndromes and oral arginine in myocardial ischemia needs to be studied further.     

Do parental convict cichlids of different sizes value the same brood number equally?

OBJECTIVES: We sought to determine endothelium-dependent vasodilator function in the brachial artery of patients with microvascular angina pectoris. BACKGROUND: Previous studies suggest the presence of endothelial dysfunction of the coronary microcirculation in patients with microvascular angina pectoris. It is not known whether endothelial dysfunction in these patients is a generalized process or whether it is confined to the coronary microcirculation only. METHODS: In 11 women (mean [+/-SD] age 60.1 +/- 7.8 years) with microvascular angina (anginal pain, normal epicardial coronary arteries, positive exercise stress test), endothelium-dependent vasodilation was assessed in the brachial artery by measuring the change in brachial artery diameter in response to hyperemic flow. Results were compared with 11 age- and gender-matched patients with known three-vessel coronary artery disease and 11 age- and gender-matched healthy control subjects. In all subjects, the intima-media thickness (IMT) of the common carotid artery was also measured. RESULTS: Flow-mediated dilation (FMD) was comparable in patients with microvascular angina and coronary artery disease (1.9 +/- 2.5% vs. 3.3 +/- 3.3%, p = NS) but was significantly lower in patients with microvascular angina than in healthy control subjects (1.9 +/- 2.5% vs. 7.9 +/- 3%, p < 0.05). IMT was significantly lower in patients with microvascular angina than in those with coronary artery disease (0.64 +/- 0.08 vs. 1.0 +/- 0.28 mm, p < 0.05) and was comparable between patients with microvascular angina pectoris and healthy control subjects (0.64 +/- 0.08 vs. 0.56 +/- 0.14 mm, p = NS). IMT > or = 0.8 mm was observed in 1 of 11 patients with microvascular angina, 1 of 11 control subjects and 10 of 11 patients with coronary artery disease. CONCLUSIONS: These findings suggest that endothelial dysfunction in microvascular angina is a generalized process that also involves the peripheral conduit arteries and is similar to that observed in atherosclerotic disease. IMT could be helpful in discriminating patients with microvascular angina and atherosclerotic coronary artery disease.     

Selective ergonovine-induced coronary artery spasm and ST-segment alternans after blunt thoracic trauma

A 24-year-old man was found to have angiographically normal coronary arteries shortly after suffering blunt thoracic trauma. Selective ergonovine administration into the left coronary artery induced total occlusion of the left anterior descending branch and electrical alternans of the ST-segment. This case demonstrates coronary artery spasm as a possible mechanism of coronary occlusion after blunt thoracic trauma.     

Soluble P-selectin is released into the coronary circulation after coronary spasm

BACKGROUND: The glycoprotein P-selectin is an adhesion molecule involved in the property change of leukocytes at the initiation of the inflammatory process. The purpose of the present study was to determine whether acute myocardial ischemia induced by coronary spasm causes an acute inflammatory response in the coronary circulation. METHODS AND RESULTS: We examined plasma soluble P-selectin levels in the coronary sinus and the aortic root simultaneously in 16 patients with coronary spastic angina before and after left coronary artery spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Ten control patients with chest pain but normal coronary arteries and no coronary spasm also received intracoronary acetylcholine. Plasma soluble P-selectin levels were increased significantly in the coronary sinus (32.8 +/- 3.6 to 52.8 +/- 5.9 ng/mL, P < .001) and in the aortic root (34.6 +/- 3.7 to 41.9 +/- 4.4 ng/mL, P < .05) after the attacks in the coronary spastic angina group but remained unchanged in the stable exertional angina group after the attacks and in the control group after the administration of acetylcholine. Furthermore, the coronary sinus-arterial difference of soluble P-selectin increased significantly after the attacks in the coronary spastic angina group (-1.8 +/- 2.2 to 10.9 +/- 2.7 ng/mL, P < .001). CONCLUSIONS: Our data indicate that soluble P-selectin is released into the coronary circulation after coronary artery spasm. We conclude that coronary artery spasm may induce the leukocyte adhesion in the coronary circulation and may lead to myocardial damage.     

Value of T-wave direction with lead III ST-segment depression in acute anterior wall myocardial infarction: electrocardiographic prediction of a "wrapped" left anterior descending artery

BACKGROUND: Lead III ST-segment depression during acute anterior wall myocardial infarction (AMI) has been attributed to reciprocal changes. However, the value of the T-wave direction (positive or negative) in predicting the site of obstruction and type of the left anterior descending (LAD) artery is not clear and has not been studied before. HYPOTHESIS: The aim of the study was to assess retrospectively the correlation between two patterns of lead III ST-segment depression, and type of LAD artery and its level of obstruction during first AMI. METHODS: The study group consisted of 48 consecutive patients, admitted to the coronary care unit for first AMI, who showed ST-segment elevation in lead a VL and ST-segment depression in lead III on admission 12-lead electrocardiogram. The patients were divided by T-wave direction into Group 1 (n = 31), negative T wave, and Group 2 (n = 17), positive T wave. The coronary angiogram was evaluated for type of LAD ("wrapped", i.e., surrounding the apex or not), site of obstruction (pre- or postdiagonal branch), and other significant coronary artery obstructions. RESULTS: Mean lead III ST-segment depression was 1.99 +/- 1.32 mm in Group 1 and 1.13 +/- 0.74 mm in Group 2 (p = 0.004); mean ST-segment elevation in a VL was 1.35 +/- 0.84 mm and 1.23 +/- 0.5 mm, respectively (p = 0.5). A wrapped LAD was found in 12 patients (38.7%) in Group 1 and in 13 in Group 2 (76.4%) (p = 0.02). The sensitivity of lead III ST-segment depression with positive T wave to predict a wrapped LAD was 52%, and the specificity was 82% with a positive predictive value of 76%. On angiography, 25 patients (80%) in Group 1 and 13 (76%) in Group 2 had prediagonal occlusion of the LAD (p = 0.77). No significant difference between groups was found for right and circumflex coronary artery involvement or incidence of multivessel disease. CONCLUSIONS: The presence of lead III ST-segment depression with positive T wave associated with ST-segment elevation in a VL in the early course of AMI can serve as an early electrocardiographic marker of prediagonal occlusion of a "wrapped" LAD.     

Defective early T and T-dependent B cell activation in systemic lupus erythematosus

Unstable coronary artery disease is a term encompassing both unstable angina and non-Q-wave (non-ST-segment elevation) myocardial infarction. Patients with these conditions are at risk of early progression to acute myocardial infarction and death. Thus, management of these conditions must aim to reduce long-term mortality and morbidity. Risk stratification is crucial for the identification of patients whose risk of early progression is high; they may require coronary angiography and (if suitable) either percutaneous transluminal coronary angioplasty or coronary artery bypass surgery. No single variable can accurately predict risk, but considerable data are emerging to show that biochemical markers of myocardial injury, such as troponin-T and troponin-I, are valuable in combination with electrocardiographic findings and clinical features. Routine early invasive procedures (coronary angiography with or without revascularization) have not yet been shown to have any significant advantage over conservative regimens for the majority of patients. Antiplatelet, anticoagulant, and anti-ischemic agents remain the mainstay of treatment in the acute phase. New agents, such as glycoprotein IIb/IIIa receptor inhibitors and low-molecular-weight heparins, as well as antithrombins and Factor Xa inhibitors add to the treatments currently available. Thrombolytic agents are contraindicated in the absence of ST-segment elevation. After clinical stabilization, ongoing assessment should include exercise testing for all patients who are able; other imaging techniques should be used for patients unable to exercise. A profile indicating a high risk of future events is an indication for elective angiography and consideration for revascularization.     

Comparison of coronary endothelial dynamics with electrocardiographic and left ventricular contractile responses to stress in the absence of coronary artery disease

Coronary artery endothelial dysfunction has been proposed as a cause of myocardial ischemia and symptoms in patients with angina-like chest pain despite normal coronary angiograms, especially those with ischemic-appearing ST-segment depression during exercise (syndrome X). We measured coronary vasomotor responses to acetylcholine (3 to 300 microg/min) in 42 patients (27 women and 15 men) with effort chest pain and normal coronary angiograms who also had normal electrocardiograms and echocardiograms at rest. All patients underwent treadmill exercise testing and measurement of systolic wall thickening responses to dobutamine (40 microg/kg/min) during transesophageal echocardiography. There were no differences in the acetylcholine-stimulated epicardial coronary diameter (+5+/-13% vs +1+/-13%, p=0.386) and flow (+179+/-90% vs +169+/-96%, p=0.756), or in the systolic wall thickening responses (+134+/-65% vs +118+/-57%, p=0.445) from baseline values in the 12 syndrome X patients compared with the 30 patients with negative exercise test results. In patients in the lowest quartile of coronary flow responses to acetylcholine, dobutamine increased systolic wall thickening by 121+/-73%; 3 had ischemic-appearing ST-segment depression during this stress. This contractile response to dobutamine was no different than the increase in systolic wall thickening (129+/-48%, p=0.777) in patients in the highest quartile of coronary flow responses, 3 of whom also had ischemic-appearing ST-segment depression during this stress. Thus, coronary endothelial dysfunction in the absence of coronary artery disease does not account for ischemic-appearing ST-segment depression in patients with chest pain despite normal coronary angiograms. Further, coronary endothelial dysfunction is not associated with myocardial contractile responses to stress consistent with myocardial ischemia.     

Somatic symptoms and panic attacks: a retrospective study of learning experiences

To determine the clinical significance of ST-segment depression observed in paroxysmal supraventricular tachycardia (PSVT), we evaluated the 12-lead electrocardiogram (ECG) during spontaneous PSVT in 54 patients (27 men and 27 women: mean age +/- SD; 47 +/- 18 years), who came to our clinic for the treatment of PSVT. Coronary angiography was performed in 16 patients (16 to 74 years; mean = 50 +/- 18) and treadmill exercise testing was performed in 21 patients. A cardiac electrophysiological study was carried out in 24 patients. During PSVT, ST-segment score was calculated as the sum of the ST-segment depression in 12 leads. The correlations between the ST-segment score, PSVT rate and age of the patient were analyzed as follows: The most significant positive correlation was observed between the ST-segment score and the PSVT rate (r = 0.615, p < 0.000001). The next most significant correlation was found between the PSVT rate and the age of the patient (r = -0.500, p = 0.00011). A negative correlation was also observed between the ST-segment score and the age of the patient (r = -0.429, p = 0.0012). In 13 of 16 patients, coronary angiography did not reveal any significant (> or = 75% in area) stenosis. Exercise testing induced significant ST-segment depression in 3 patients, of whom two had significant coronary artery lesions. PSVT was due to atrioventricular reentry via an overt (n = 3) or concealed accessory pathway (n = 15), atrioventricular nodal reentry (n = 5) and sinus node reentry (n = 1). In conclusion, patients with a faster PSVT rate revealed more pronounced ST-segment depression than did those with a slower PSVT rate, possibly reflecting the modified repolarization process instead of coronary artery involvement.     

Diabetics with coronary disease have a prevalence of asymptomatic ischemia during exercise treadmill testing and ambulatory ischemia monitoring similar to that of nondiabetic patients. An ACIP database study. ACIP Investigators. Asymptomatic Cardiac Ischemia Pilot Investigators

BACKGROUND: There are conflicting data as to whether diabetics have a higher prevalence of asymptomatic ST-segment depression during exercise treadmill testing (ETT) and ambulatory ECG (AECG) monitoring. This study was conducted to determine whether diabetic patients with coronary disease enrolled in the Asymptomatic Cardiac Ischemia Pilot (ACIP) have more episodes of asymptomatic ischemia during ETT and 48-hour AECG monitoring than nondiabetic patients and to compare differences in angiographic variables and the magnitude of ischemia as measured by standard ETT and AECG criteria. METHODS AND RESULTS: Angiographic variables and the prevalence and magnitude of ischemia during the qualifying ETT and 48-hour AECG were compared by the presence and absence of diabetes mellitus in 558 randomized ACIP patients. Seventy-seven patients had a history of diabetes and were taking oral hypoglycemics or insulin (diabetic group); 481 patients did not meet these criteria (nondiabetic group). Multivessel disease (87% versus 74%, P = .01) was more frequent in the diabetic group. The percentages of patients without angina during the ETT were similar in the diabetic and nondiabetic groups (36% and 39%, respectively). Time to onset of > or = 1-mm ST-segment depression and time to onset of angina were similar in both groups. The percentages of patients with only asymptomatic ST-segment depression during the 48-hour AECG were similar in the diabetic and nondiabetic groups (94% versus 88%, respectively). However, total ischemic time per 24 hours (15.0 +/- 21.4 versus 23.6 +/- 31.1 minutes, P = .02), ischemic time per episode (6.3 +/- 4.6 versus 9.0 +/- 8.7 minutes, P < .01), and the maximum depth of ST-segment depression tended to be less in the diabetic group. CONCLUSIONS: Patients enrolled in ACIP were selected on the basis of an abnormal ETT and 48-hour AECG and ability to undergo coronary revascularization. When patients with diabetes mellitus were compared with those without diabetes, there was a similar prevalence of asymptomatic ischemia during ETT and 48-hour AECG monitoring. Despite more extensive and diffuse coronary disease, diabetic ACIP patients tended to have less measurable ischemia during the 48-hour AECG.     

Quantum chemical studies of methadone

To clarify the association between chest pain and significant coronary artery disease in patients who have aortic valve disease, 76 consecutive candidates for aortic valve replacement were evaluated prospectively with use of a historical questionnaire and coronary arteriography. Of the 76 patients, 19 (25 percent) had no chest pain, 21 (28 percent) had chest pain that was not typical of angina pectoris and 36 (47 percent) had chest pain typical of anigina pectoris. In 18 of 19 patients the absence of chest pain correlated with the absence of coronary artery disease. The single patient without chest pain who had coronary artery disease had evidence of an inferior myocardial infarction in the electrocardiogram. Thus, absence of chest pain and the absence of electrocardiographic evidence of infarction predicted the absence of coronary disease in all cases. The presence of chest pain did not predict the presence of coronary artery disease, but the more typical the pain of angina pectoris the more likely were patients to have significant coronary artery disease. Of the 21 patients with atypical chest pain, 6 (29 percent) had coronary artery disease, but of the 36 patients with typical angina pectoris 23 (64 percent) had significant coronary artery disease. In addition, when patients with chest pain not typical of angina pectoris also had coronary artery disease, the diseased vessels usually supplied smaller areas of the left ventricle than when the pain was typical of angina pectoris. In 21 of 23 patients (91 percent) with typical angina pectoris and significant coronary artery disease, lesions were present in the left coronary artery. There was no systolic pressure gradient across the aortic valve that excluded the presence of coronary artery disease, although all patients with a calculated aortic valve area of less than 0.4 cm2 were free of coronary artery disease. Patients with severe left ventricular dysfunction were more likely to have normal coronary arteries.     

ST segment changes in the ECG. Anesthesia induction with propofol, etomidate or midazolam in patients with coronary heart disease

Induction of anaesthesia with propofol and fentanyl can lead to marked reductions in mean arterial pressure (MAP) and heart rate (HR). Thus, the application of propofol in patients with severely reduced coronary artery perfusion is controversial. METHODS. The study group consisted of 60 patients undergoing coronary artery bypass grafting (CABG). Anaesthesia was induced over 30 s with propofol (P 1.5 mg/kg), etomidate (E 0.3 mg/kg), or midazolam (M 0.15 mg/kg) following a bolus dose of fentanyl (5 micrograms/kg). Vecuronium was used as a muscle relaxant. During induction we continuously measured MAP and HR and recorded the occurrence of myocardial ischaemia using an automatic ST-segment analyser (Marquette 7010). ST-segment deviations of more than 1 mm in leads II and V5 were interpreted as significant signs of myocardial ischaemia. RESULTS. All groups showed reductions in MAP and HR on induction that were marked in the P group. Intubation caused elevation of MAP and HR to pre-induction levels (HR: all groups) or slightly above (MAP: E, M). Four patients in the P group and 3 in each other group showed significant ST-segment deviation prior to induction. In the P group these deviations disappeared in 2 patients after injection while they remained unchanged in the M group. In the E group injection had no effect on the ischaemic ECG changes but produced another case of significant ST-segment deviation. Laryngoscopy and intubation produced no further significant ST-segment deviation in either group. DISCUSSION. Induction is a critical phase of anaesthesia, especially in patients with limited coronary reserve. Induction agents should alleviate the stress response while causing minimal haemodynamic changes. Despite marked reductions in MAP in the P group, the number of patients with ischaemic ECG changes was cut by half. Their number was unchanged or even raised in the other groups. After application of P, with an alleged reduction of coronary perfusion, a compensational reduction in myocardial oxygen consumption may occur.     

Early experience with dobutamine stress testing and cardiac cine-tomographic imaging in the elderly: antianginal effects of nifedipine-GITS

OBJECTIVE: To determine the effects of nifedipine-GITS (GITS = gastrointestinal transport system) on angina and cardiovascular responses to stress-dobutamine infusion, we used ultrafast cine-computed tomography (CT) to assess regional wall motion, myocardial perfusion, and indices of ventricular filling and emptying. DESIGN: Randomized, double-blind placebo-controlled efficacy study after an open-label dose titration phase. SETTING: University of California, San Francisco. PATIENTS: Elderly patients (> 60 years; n = 9:8 male, 1 female) with coronary artery disease by history and diagnostic treadmill or coronary angiography. INTERVENTION: After a 3-week open-label dose-titration phase, eight subjects were randomized to receive either placebo or nifedipine-GITS at the highest tolerated dose for 2 weeks, followed by a crossover to the alternate therapy for 2 weeks. One declined because of singulus in the open-label period. MAIN OUTCOME MEASURES: Symptomatic angina relief (frequency and nitroglycerin consumption), dobutamine stress responses (time to ischemia during dobutamine infusions, cardiac output, cardiac ejection fraction, ventricular segmental wall motion, and perfusion as measured by ultrafast cine-CT), and reported adverse effects. RESULTS: When compared with placebo, nifedipine-GITS administration was associated with less frequent angina and nitroglycerin consumption (NS) and significantly decreased systolic blood pressure. Nifedipine-GITS administration also increased resting supine heart rates. Dobutamine infusions increased heart rate, cardiac output, cardiac ejection fraction, and stroke volume and induced angina symptoms. Neither double product at angina nor systolic indices of cardiac function in response to dobutamine differed between nifedipine-GITS and placebo, although heart rate responses were greater during nifedipine. A trend toward increased peak filling rates was seen during dobutamine stress in the nifedipine-administration period. In most subjects (6/8), perfusion and regional wall motion abnormalities were not visualized on regional wall motion abnormalities were not visualized on either rest or stress cine-CT studies. Edema without congestive heart failure occurred frequently during nifedipine-GITS administration. CONCLUSIONS: These data suggest that (1) dobutamine stress can be used to induce cardiac ischemia in elderly patients with coronary artery disease, (2) nifedipine-GITS provides symptomatic angina relief in elderly patients, (3) peripheral edema is frequent in elderly patients on nifedipine-GITS, and (4) ultrafast computed cine-tomography testing can be used to assess ventricular performance, but current methodology may not detect perfusion or wall motion abnormalities during angina.