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PubMed1989

Quantitative arteriographic responses to ergonovine provocation in subjects with atypical chest pain.

To evaluate the nonspecific vasoconstrictor response to intravenous ergonovine, and identify patient-related factors that systematically alter changes in coronary dimensions, 33 subjects (22 women, 11 men), mean age 54 years (range 39 to 70) were studied using a standardized ergonovine provocation test (Stanford protocol). Clinical responses, systemic hemodynamics and electrocardiographic changes were determined, with quantitative arteriography used for sequential measurement of proximal right coronary dimensions. A progressive decrease in proximal right coronary diameter was observed, with average control values and final diameters equaling 3.25 +/- 0.49 and 2.56 +/- 0.49 mm, respectively, thus representing an overall -21.2% change from baseline. No significant differences existed in control dimensions when analyzed with respect to gender (3.20 +/- 0.59 vs 3.40 +/- 0.72 mm, women vs men, difference not significant), although women demonstrated a greater decrease from baseline values (0.80 +/- 0.30 vs 0.50 +/- 0.24 mm, women vs men, p less than 0.05). The presence of minor atherosclerotic disease, as determined by the presence of minor (less than 30% diameter) luminal irregularities within the right coronary artery, failed to alter control dimensions (3.30 +/- 0.48 vs 3.20 +/- 0.51 mm, normal vs atherosclerotic persons, difference not significant), but was associated with more ergonovine-induced coronary vasospasm (0.41 +/- 0.27 vs 0.84 +/- 0.21 mm, normal vs atherosclerotic persons, p less than 0.01). Therefore, sequential intravenous ergonovine maleate infusion resulted in progressive, nonspecific reductions in proximal right coronary artery dimensions in subjects without a history compatible with vasospastic angina. This nonspecific vasoconstrictor effect was accentuated in women and subjects with intimal irregularities suggestive of minor atherosclerotic coronary disease.

Adult↗
PubMed1990

Doppler assessment of left ventricular filling pattern in silent ischemia in patients with Prinzmetal's angina.

Spontaneous angina is an ideal condition in which to study left ventricular (LV) dysfunction induced by acute myocardial ischemia. In 6 patients with Prinzmetal's angina, LV diastolic function during 16 episodes of spontaneous angina was studied by simultaneous recordings of electrocardiographic (ECG), echocardiographic and hemodynamic parameters. In particular, pulsed Doppler echocardiography measured peak velocity of early (E) and late (A) transmitral flow and E/A ratio, as indexes of relative early versus late LV filling. During the ischemic attacks, the time sequence of pulsed Doppler echocardiographic and ECG changes showed 3 distinct phases: (1) "waxing phase: transmitral flow changes with minimal ECG modifications (E/A = 0.85 +/- 0.1); (2) "steady" phase: maximal ECG changes (E/A = 0.9 +/- 0.1); and (3) "waning" phase: regression of the ECG changes (E/A = 1.26 +/- 0.15). In each phase, E/A ratio showed a significant difference from the baseline value (E/A = 1.17 +/- 0.2) as a result of changes in E, suggesting that myocardial ischemia affects mainly the early phase of diastole. In the waxing phase, LV diastolic dysfunction preceded systolic abnormalities, as documented by a significant reduction of E/A ratio in the absence of alterations in LV ejection fraction, as well as in systemic arterial and pulmonary wedge pressures. Finally, all the recorded parameters were consistent with LV "contractile rebound" occurring in the waning phase and affecting both diastole and systole.

Angina Pectoris, Variant↗
PubMed1991

Felodipine (once daily) versus nifedipine (four times daily) for Prinzmetal's angina pectoris.

In 30 consecutive patients with Prinzmetal's angina pectoris, the antiischemic effect of felodipine, a new long-acting vasoselective calcium antagonist, administered at doses of 10 and 20 mg once daily was compared with that of the well-established therapeutic regimen with nifedipine administered at a dose of 20 mg 4 times daily. Twenty-four-hour Holter monitoring was performed during a 2-day placebo run-in and at the end of each of 3 consecutive 6-day periods during which the 3 active treatments were administered in randomized sequence. Three patients withdrew, whereas 27 completed the study. The therapeutic regimens tested proved to be similarly effective; primary end points (ischemic episodes recorded by Holter monitoring, and anginal attacks reported on diary cards) occurred in 5 patients (19%) during nifedipine treatment, and in 7 (26%) and 3 (11%) during felodipine treatment with 10 and 20 mg, respectively (p = not significant). The distribution of residual ischemic episodes demonstrated that treatment with felodipine once daily provides 24-hour antiischemic protection. Twenty-six patients were followed up with 20 mg of felodipine once daily for a mean of 6 +/- 5 months, and 21 of them (81%) remained free of symptoms and Holter-recorded ischemic attacks. It is concluded that for Prinzmetal's angina pectoris, 24-hour antiischemic protection may be achieved with administration of felodipine once daily. The availability of a simplified therapeutic approach may constitute a real advantage in terms of patient compliance and improving the quality of life.

Angina Pectoris, Variant↗
PubMed1992

Tissue plasminogen activator using a rapid-infusion low-dose regimen for unstable angina.

The clinical effect of a low-dose rapid-infusion intravenous regimen was assessed using human recombinant tissue-type plasminogen activator (rt-PA) in unstable angina. Fifty patients with unstable angina pectoris were randomly assigned to blinded treatment with either placebo (24 patients) or low-dose (20 mg bolus, 30 mg infusion over 1 hour) intravenous rt-PA (26 patients). Before randomization, all patients were treated with aspirin, twice-daily subcutaneous heparin, and maximally tolerated antianginal therapy. Of the 50 patients assigned, 26 received rt-PA and the outcome was successful in 15 (58%) (angina settled, no myocardial infarction or urgent intervention) compared with 9 (38%) successful outcomes in the 24 who received placebo (0.5 greater than p greater than 0.1). Angina remained refractory in 8 (31%) of the rt-PA group and in 13 (54%) of the placebo group (0.1 greater than p greater than 0.05). Urgent interventions were required in 6 patients (23%) who received rt-PA and in 11 patients (46%) who received placebo. Three patients in each group sustained a myocardial infarction within 72 hours of entering the trial and there were 3 deaths (1 in the active treatment group, 2 in placebo group) within 2 weeks of the trial (p = not significant). Administration of intravenous rt-PA was not associated with any complications. Low-dose rt-PA administration in patients with unstable angina was associated with a tendency to stabilization of anginal symptoms and a reduction in the need for urgent intervention. However, these trends did not achieve statistical significance.

Aged↗
PubMed1994

Usefulness of amlodipine for angina pectoris.

Calcium antagonists are effective antianginal agents in the treatment of patients with stable exercise-induced angina pectoris. A series of randomized, double-blind, placebo-controlled studies with the novel, once-daily calcium antagonist amlodipine have been completed in a large number of patients with stable exercise-induced angina pectoris. Compared with placebo, once-daily amlodipine demonstrated a significant dose-related extension in exercise duration and workload accomplished, and reduction in number of anginal attacks and associated glyceryl trinitrate consumption. The clinical antianginal attributes of amlodipine were accompanied by significant reductions in electrocardiographic evidence of myocardial ischemia. In comparison with other antianginal drugs, once-daily amlodipine at a dosage range of 5-10 mg demonstrated antianginal activity comparable to thrice-daily diltiazem and once-daily nadolol. Amlodipine administered once daily achieves symptomatic and electrocardiographic amelioration of myocardial ischemic episodes induced by exercise in the majority of patients with stable angina pectoris. Amlodipine does not depress left ventricular pumping activity, and its side-effect profile does not differ substantially from that of placebo.

Amlodipine↗
PubMed1994

Vasomotor response to ergonovine of epicardial and resistance coronary arteries in the nonspastic vascular bed in patients with vasospastic angina.

The hypothesis that a coronary vasomotion disorder may exist in the entire coronary artery tree in patients with vasospastic angina was investigated by examining the coronary responses to atrial pacing (130 beats/min) before and after the administration of ergonovine (16 micrograms) into nonspastic coronary arteries. Seven patients with angiographically normal coronary arteries and focal spasm in the right coronary artery and 7 control patients with atypical chest pain and angiographically normal coronary arteries without spasm were studied. Great cardiac vein flow (GCVF) and left anterior descending coronary artery diameters (CDs) were measured by the thermodilution method and quantitative arteriography, respectively. Although the CDs before ergonovine were similar in the 2 groups, the pacing-induced increased in GCVF before ergonovine administration was smaller in patients with vasospastic angina than in control patients (22 +/- 4% vs 49 +/- 11%, respectively; p < 0.05). After ergonovine administration, pacing both increased GCVF and decreased anterior regional coronary resistance (ACR) to a lesser extent in patients with vasospastic angina than in control patients (GCVF, 16 +/- 4% vs 47 +/- 8%, respectively [p < 0.01]; ACR, -12 +/- 3% vs -29 +/- 3%, respectively [p < 0.01]). The decreases in CDs in patients with vasospastic angina observed after ergonovine administration were greater than those in control patients (-18 +/- 2% vs -9 +/- 2%, respectively; p < 0.05). Thus, not only epicardial, but also resistance coronary arteries are affected by the coronary vasomotion disorder in the nonspastic vascular bed in patients with vasospastic angina.

Adult↗
PubMed1976

Prinzmetal's angina with coronary artery spasm. Angiographic, pharmacologic, metabolic and radionuclide perfusion studies.

We studied the effects of coronary artery spasm on perfusion of the microvasculature in a patient with Prinzmetal's angina. Intracoronary injections of 99mTc and 131I-labelled macroaggregated human serum albumin were performed (1) at rest, (2) during spontaneous angina, (3) after the administration of nitroglycerin and (4) during pacing-induced spasm and the resultant scans compared. The resting scan was normal. Pain and spasm were associated with a perfusion defect that was localized to the anterior and inferior walls of the left ventricle. The localization of the perfusion defect corresponded with angiographically demonstrated spasm involving left anterior descending and distal circumflex coronary arteries. A subsequent myocardial infarction was localized by 43K scanning to the same perfusion area. Metabolic and parasympathetic stimulation studies were performed but were inconclusive. The patient's recurrent pains were ultimately controlled with large oral doses of isosorbide dinitrate.

Angina Pectoris↗
PubMed1978

Rest angina with transient S-T segment elevation. Correlation of clinical features with coronary anatomy.

In 44 consecutive patients with angina at rest associated with transient S-T segment elevation, clinical features were correlated with angiographic coronary anatomy. Patients were divided into three groups depending on the number of major vessels having greater than or equal to 70 per cent luminal narrowing: Group I = no or minimal disease (six patients); group II = single vessel disease (13 patients); and group III = multiple vessel disease (25 patients). The following features did not differ significantly among groups I, II or III: age, sex, risk factors, time from onset of episodes of pain at rest to study or arrhythmias during ischemic episodes. Patients in group III were more likely to have angina on effort (p less than 0.001) and an abnormal base line electrocardiogram (p less than 0.001) than patients in groups I or II. However, the absence of these features did not separate patients in group I from those in group II. In patients with angina at rest associated with transient S-T segment elevation, clinical features identify patients with multiple vessel disease but do not allow differentiation of patients with no or minimal coronary disease from patients with single vessel disease.

Adult↗
PubMed1981

Coronary arterial spasm versus esophageal spasm. Response to ergonovine.

In this report we show that coronary arterial and esophageal spasm are sometimes clinically indistinguishable. Pain patterns can be identical, nitroglycerin can bring relief, interval electrocardiograms and exercise electrocardiograms generally disclose no abnormalities, coronary arteriograms may be within normal limits or nearly so, and, importantly, an ergonovine provocative test can provoke esophageal spasm accompanied by pain mistaken for Prinzmetal's angina. Accordingly, chest pain in response to the administration of ergonovine is not evidence of coronary arterial spasm without simultaneous arteriographic proof together with changes in the monitoring electrocardiogram. Conversely, gastroenterologists should not expose patients to the risk of ergonovine without prior assurance that the coronary arterial response is normal. Our observations illustrate these points and identify a patient with symptomatic esophageal spasm previously diagnosed as Prinzmetal's angina.

Angina Pectoris↗
PubMed1981

Coronary artery spasm in the denervated transplanted human heart: a clue to underlying mechanisms.

The mechanism of coronary artery spasm has been poorly understood but there has been some suggestion that cardiac autonomic innervation may play an important role. We report coronary artery spasm in a 43 year old man two years after he had received a transplant. Provocative pharmacologic testing suggested functional denervation of the patient's heart. Thus, coronary artery spasm can occur in the transplanted, denervated human heart. Autonomic innervation of the heart is not essential in all cases of coronary spasm, and circulating catecholamines and/or metabolic of hormonal products may play an important role.

Adolescent↗
PubMed1982

Therapeutic and economic value of a normal coronary angiogram.

A significant number of patients with severe angina or intractable atypical chest pain referred for coronary arteriography are found to have normal coronary vessels. To determine what therapeutic or economic benefit may be derived from these studies, we analyzed the data of 72 consecutive patients with normal vessels referred for cardiac catheterization because of severe chest pain. The clinical status and hospitalizations were analyzed for the 2 year period before and the 2 year period after angiography. There were no deaths or myocardial infarctions. Although 47 were thought to have angina and 25 atypical pain before catheterization, the chest pain was reclassified with only 15 continuing to have anginal pain, 40 atypical pain, and 17 no pain. Functional improvement by at least one New York Heart Association class occurred in 74 percent of patients with 36 (50 percent) having no functional limitation. The use of cardiac medications was also significantly reduced. Despite functional improvement, no change in employment states could be demonstrated. The use of medical facilities was significantly less, the average number of hospital days per patient declining from 17 to 3.9 and hospitalization decreasing from 1.5 to 0.4. The result was a significant decrease in estimated hospital costs. We conclude that in patients referred for coronary angiography for severe chest pain, documentation of a normal coronary arteriogram significantly alters the clinical assessment of symptoms, improves functional status, modifies medical therapy, and reduces hospitalization and medical costs. These therapeutic and economic benefits deserve consideration in the evaluation of coronary angiography for its overall effectiveness.

Adult↗
PubMed1982

Serum estrogen levels in men with acute myocardial infarction.

Serum estradiol and serum estrone levels were assessed in 29 men in 14 men in whom myocardial infarction was ruled out; in 12 men without apparent coronary heart disease but hospitalized in an intensive care unit; and in 28 men who were not hospitalized and who acted as control subjects. (The 12 men who were hospitalized but who did not have coronary heart disease were included to control for physical and emotional stress of a severe medical illness.) Ages ranged from 21 to 56 years. Age, height, and weight did not differ significantly among groups. Blood samples were obtained in the patient groups on each of the first three days of hospitalization. The serum estrone level was significantly elevated in all four patient groups when compared with that in the control group. Estrone level, then, did not differentiate patients with and without coronary heart disease. Serum estradiol levels were significantly elevated in the groups with myocardial infarction, unstable angina, and in the group in whom myocardial infarction was ruled out. However, estradiol levels were not significantly elevated in the group in the intensive care unit without coronary heart disease when compared to the level in the normal control group. Serum estradiol levels, then, were elevated in men with confirmed or suspected coronary heart disease but were not elevated in men without coronary heart disease even under the stressful conditions found in an intensive care unit. Serum estradiol levels were significantly and positively correlated (p less than 0.03) with serum total creatine phosphokinase levels in the patients with myocardial infarction. The five patients with myocardial infarction who died within 10 days of admission had markedly elevated serum estradiol levels. The potential significance of these serum estradiol elevations is discussed in terms of estradiol's ability to enhance adrenergic neural activity and the resultant increase in myocardial oxygen demand.

Adult↗
PubMed1982

Multiclinic controlled trial of diltiazem for Prinzmetal's angina.

To assess the efficacy of a new calcium entry blocker, diltiazem (Cardizem), for prophylaxis of Prinzmetal's angina, 48 patients were studied in randomized, multiple crossover multiclinic study (2 weeks single-blind, 8 weeks double-blind). Diltiazem dosage in one crossover phase was 120 mg per day; in the other, 240 mg per day. Therapeutic response was measured by patients' diary records of angina frequency and nitroglycerin tablet consumption. Treatment with 120 mg of diltiazem per day reduced angina by 41 percent from the entry placebo period and 20 percent from the paired placebo period (p less than 0.005). Treatment with 240 mg of diltiazem per day reduced angina frequency by 68 percent from the entry placebo period and 43 percent from the paired placebo period (p less than 0.01). There were similar reductions in nitroglycerin consumption. Adverse experiences that may have been related to the medication were noted in only 5 percent of patients. There were no alterations in blood pressure or heart rate. The PR interval increased 3 percent at the 240 mg dosage level. We conclude that diltiazem is an effective and safe agent for control of symptoms of Prinzmetal's angina.

Adult↗
PubMed1983

Titrates for treatment of unstable angina pectoris and coronary vasospasm.

The treatment of a patient with unstable angina at the time of the initial presentation of the physician can begin with nitrates. The beneficial action of nitrates are several. Nitrates dilate epicardial coronary arteries as well as many coronary artery stenoses. They may be effective because of this action plus a marked effect on decreasing ventricular volume and ventricular end diastolic pressure. Perhaps the best way to manage patients with severe angina that may be in part related to coronary artery vasoconstriction is to combine a long-acting nitrate with a calcium antagonist. The combined use of nitrates and calcium antagonists will (1) dilate the coronary arteries to maintain coronary blood flow, (2) decrease systemic arterial pressure and thus decrease peripheral vascular resistance, and (3) dilate peripheral veins and thus decrease ventricular volume and pressure. When proper doses are used, the combination may be more effective than either drug alone. Of course, proper dosing must be determined for the individual patient by the physician. Initial treatment with the nitrates should begin with small doses and gradually build up. Similar dosing schedules should be used for the calcium antagonists. Both doses can be increased to high levels is the clinical situation warrants it.

Adrenergic beta-Antagonists↗