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PubMed1995

[Clinical aspects and classification of unstable angina].

Unstable angina pectoris is a clinical syndrome with multiple underlying pathophysiologic mechanisms. This presentation is concerned with primary angina pectoris exclusively. In the majority of cases a rupture of an atherosclerotic plaque and an intracoronary thrombus are responsible for instable angina. The practitioner's role is to identify those patients who will develop complications with the aid of clinical parameters. Prinzmetal's angina is also instable, occurs at rest and leads to ST-segment elevation. It is most likely due to coronary spasm, developing in disease-free and atherosclerotic coronary segments alike. This variant of unstable angina is treated most successfully with calcium antagonists. The recognition of the responsible pathophysiologic mechanism permits adjustment of treatment of every patient taking into consideration the seriousness of his prognosis.

Angina Pectoris, Variant↗
PubMed1976

Prinzmetal's variant angina.

Two patients are described with a typical Prinzmetal's variant angina. Both patients were young, active males with angina of recent onset. They experienced angina only at rest and in one patient the angina had a cyclic character appearing only between 4 and 10 a.m. In both patients there was no correlation whatsoever between the angina pectoris and effort, emotion or change in temperature and the angina reacted promptly to nitroglycerine sublingually. The number of attacks and the intensity of the pain were increasing rapidly over a short period of time in both cases. The stenoses in both patients did not exceed 50% of the lumen of the coronary arteries, but coronary surgery has been performed on clinical grounds because both patients were completely disabled and one of them suffered from life-threatening dysrhythmias. For respectively 18 and 6 months after saphenous vein bypass surgery both patients have been symptom-free and able to resume their work. The problems concerning the diagnosis Prinzmetal's variant of angina pectoris are discussed.

Adult↗
PubMed1988

[New-onset stenocardia: the detection of clinical variants of ventricular arrhythmia].

A total of 130 patients with angina of new onset (ANO), i.e. first three months after the onset of anginal attacks, were investigated by means of 24- and 48-hour Holter's electrocardiographic monitoring. All the patients underwent selective coronarography. Ventricular arrhythmias (isolated and paired extrasystoles, ventricular tachycardias) and their correlation to acute myocardial ischemia were analysed. Ventricular tachycardia was more common in unstable ANO, as compared to stable angina, and in patients with signs of coronary spasm, as compared to anginal patients showing no such signs. The combination of unstable angina with signs of coronary spasm is the least favorable ANO variant in terms of the risk of grave ventricular arrhythmias.

Adult↗
PubMed1994

Influence of exercise-induced coronary artery spasm on thallium-201 initial distribution and washout kinetics in patients with variant and classic angina pectoris.

Thallium-201 single-photon emission computed tomography was performed immediately, and 2 and 4 hours after exercise-induced anginal attack in 2 groups of patients with either exercise-induced coronary spasm or severe fixed stenosis on the isolated proximal left anterior descending coronary artery. All patients with variant angina had transient ST-segment elevation during the exercise-induced attack for thallium-201 scintigraphic study. Both perfusion defects and 4-hour washout abnormalities were significantly greater in patients with variant angina than in those with stable effort angina (p < 0.01). In patients with stable effort angina, thallium-201 activity in ischemic regions (as a percentage of initial count in the normal region) progressively decreased, whereas in patients with variant angina it increased from 38% (initial) to 48% (2 hours), and then declined to 42% (4 hours). The initial normalized thallium-201 activity in the ischemic regions was significantly lower in patients with variant angina than in those with stable effort angina (p < 0.001). In conclusion, perfusion and washout abnormalities during exercise-induced angina are greater in patients with variant angina than in those with stable effort angina. Exercise-induced coronary spasm seems to contribute to the profound reduction in initial thallium-201 distribution and delayed thallium-201 accumulation in the ischemic region.

Adult↗
PubMed1989

Calcium antagonists in the treatment of Prinzmetal's angina and unstable angina pectoris.

Calcium antagonists block the entry of calcium into vascular smooth muscle cells, producing pharmacological vasodilation. Thus, it is not surprising that these drugs are effective in treating unstable angina that is often characterized by increased vasomotion and dynamic obstruction at the site of atheromatous plaques. Nifedipine, diltiazem, and verapamil are all highly and equally effective in reducing painful and painless ischemic episodes in Prinzmetal's variant angina. In patients with unstable angina who have known or suspected significant underlying coronary artery disease, a multipharmacological approach to therapy is warranted. Nifedipine used with beta-blocker drugs is more effective than nifedipine as monotherapy. Diltiazem and verapamil have been shown to be effective when given without beta-blockers in unstable angina patients. In many patients, thrombus formation rather than vasospasm is the major pathophysiological event resulting in progression of the syndrome to infarction or sudden death. In these patients, antiplatelet, antithrombotic, or antiplatelet and antithrombotic therapy is of utmost importance to maintain adequate coronary flow. Nonresponders to medical therapy with unstable angina have a high prevalence of eccentric and multiple coronary stenoses with a high incidence of thrombi. The best responders to calcium antagonist therapy are patients with concentric coronary stenoses. In summary, calcium antagonists are highly effective in reducing ischemic episodes in patients with Prinzmetal's angina and effective for therapy for unstable angina when used in conjunction with other forms of medical treatment aimed at the processes of platelet activation and thrombus formation.

Adrenergic beta-Antagonists↗
PubMed1998

[Tryptase levels are elevated during spontaneous ischemic episodes in unstable angina but not after the ergonovine test in variant angina].

Activated mast cells are present in human coronary atheromas, as well as in the adventitia of patients with variant angina, and may play an important role in plaque rupture and coronary vasomotion. To assess whether or not activation of mast cells is a primary event, we measured serum levels of tryptase, a specific marker of mast cell activation, in 8 patients with unstable angina during a spontaneous ischemic episode (Group 1) and in 5 patients with variant angina (Group 2) during ergonovine-induced coronary spasm. Blood samples were collected as soon as possible after the onset of pain and ECG changes (0 min), and after 5, 15 and 60 min. Tryptase levels in Group 1 were 0.13 U/l (range 0.017-0.44) at the onset of pain and significantly raised to 0.75 U/l (range 0.05-2.49) at 5 min, decreasing to 0.076 U/l (range 0.018-0.16) at 15 min and to 0.085 U/l (range 0.01-0.25) at 60 min (p = 0.035). Conversely, tryptase levels in Group 2 were 0.09 U/l (range 0.07-0.13) at 0 min, 0.11 U/l (range 0.07-0.22) at 5 min, 0.10 U/l (range 0.07-0.18) at 15 min, 0.11 U/l (range 0.07-0.17) at 60 min (NS). In conclusion, tryptase levels raise during spontaneous ischemic episodes in unstable angina, but not after ergonovine-provoked ischemia in variant angina, suggesting that a primary, yet unknown stimulus, may activate mast cells during some ischemic episodes in unstable angina.

Aged↗
PubMed1977

Clinical medicine review: three unique presentations of ischemic heart disease.

Unstable angina pectoris, Prinzmetal variant angina, and ischemic heart disease with normal coronary arteries, are three unique syndromes of ischemic heart disease that have recently become better understood. With the recognition of their manifestations, the combination of modern medical techniques and collaborative epidemiological studies should eventually lead to their early diagnosis, optimal treatment, and possible prevention.

Acute Disease↗
PubMed1986

[Spontaneous precordial pain: coronary spasm or esophageal pathology?].

Chest pain due to esophageal spasm or esophagitis may mimic pain of variant angina. Differential diagnosis of the two diseases is often difficult and requires various tests, the value of which is discussed. These problems are illustrated by three cases. The esophageal investigation should preferably be preceded by coronary arteriography. Chest pain or dysphagia due to iced drinks is not specific for esophageal spasm but may be due to coronary spasm.

Adult↗
PubMed1996

Plasma protein acute-phase response in unstable angina is not induced by ischemic injury.

BACKGROUND: Elevated levels of C-reactive protein (CRP) are associated with an unfavorable clinical outcome in patients with unstable angina. To determine whether ischemia-reperfusion injury causes this acute-phase response, we studied the temporal relation between plasma levels of CRP and ischemic episodes in 48 patients with unstable angina and 20 control patients with active variant angina, in which severe myocardial ischemia is caused by occlusive coronary artery spasm. METHODS AND RESULTS: Blood samples were taken on admission and subsequently at 24, 48, 72, and 96 hours. All patients underwent Holter monitoring for the first 24 hours and remained in the coronary care unit under ECG monitoring until completion of the study. On admission, CRP was significantly higher in unstable angina than in variant angina patients (P < .001). In unstable angina, 70 ischemic episodes (1.5 +/- 2 per patient) and in variant angina 192 ischemic episodes (9.6 +/- 10.7 per patient) were observed during Holter monitoring (P < .001), for a total ischemic burden of 14.8 +/- 30.2 and 44.4 +/- 57.2 minutes per patient, respectively (P < .001). The plasma concentration of CRP did not increase in either group during the 96 hours of study, even in patients who had episodes of ischemia lasting > 10 minutes. CONCLUSIONS: The normal levels of CRP in variant angina, despite a significantly larger number of ischemic episodes and greater total ischemic burden, and the failure of CRP values to increase in unstable angina indicate that transient myocardial ischemia, within the range of duration observed, does not itself stimulate an appreciable acute-phase response.

Acute-Phase Reaction↗
PubMed1984

Clinical pharmacology of calcium antagonists.

Verapamil, nifedipine, and diltiazem are effective in the treatment of stable effort angina and angiospastic (variant) angina. In addition, there is evidence that the agents are beneficial in patients diagnosed as having unstable angina. The efficacy of calcium antagonists for the treatment of effort angina appears to be augmented by combining them with beta-adrenergic blockers. Intravenous verapamil, but not nifedipine, is very effective in terminating paroxysmal supraventricular tachycardias caused by re-entrant mechanisms with or without involvement of accessory pathways (WPW syndrome). Verapamil is also effective in slowing the ventricular response to atrial fibrillation or flutter. The use of verapamil for the treatment of ectopic atrial or ventricular dysrhythmias is less well established and will require further evaluation.

Angina Pectoris↗
PubMed1996

Intracellular neutrophil myeloperoxidase is reduced in unstable angina and acute myocardial infarction, but its reduction is not related to ischemia.

OBJECTIVES: This study sought to assess neutrophil activation in acute coronary syndromes and its relation to ischemic episodes. BACKGROUND: Neutrophil activation has been reported in unstable angina and acute myocardial infarction; however, it is not clear whether it is related exclusively to ischemia-reperfusion injury. METHODS: We measured the index of intracellular myeloperoxidase in 1) patients with unstable angina, myocardial infarction, variant angina and chronic stable angina and in normal subjects (protocol A); and 2) in patients with unstable angina and acute myocardial infarction during the first 4 days of the hospital period (protocol B). To assess whether neutrophil activation was triggered by ischemia, the myeloperoxidase intracellular index was analyzed before and after spontaneous ischemic episodes and before and after ischemia induced by an exercise stress test in 10 patients with chronic stable angina. In 11 patients with unstable angina, we also compared values of the myeloperoxidase intracellular index at entry with those after waning of symptoms. RESULTS: In protocol A, the myeloperoxidase intracellular index was significantly reduced in patients with unstable angina and acute myocardial infarction compared with patients with stable and variant angina and normal subjects (p < 0.01). In protocol B, the myeloperoxidase intracellular index did not change over time in patients with unstable angina and myocardial infarction. However, in 11 patients with waning symptoms, the myeloperoxidase intracellular index was significantly higher afer symptoms had waned (p < 0.05). In patients with unstable angina, 23 ischemic episodes were studied; no changes in the myeloperoxidase intracellular index were observed. In 10 patients with chronic stable angina and positive exercise stress test results, no significant differences in the myeloperoxidase intracellular index were observed after stress-induced ischemia. CONCLUSIONS: Our study confirms that neutrophils are activated in acute coronary syndromes but suggests that their activation may not be only secondary to ischemia-reperfusion injury.

Adult↗
PubMed1987

Use of nitrates in the treatment of unstable and variant angina.

Unstable angina is a clinical syndrome that includes patients with new onset of angina, a change in a previous stable pattern, or the development of chest pain at rest. Generally, more than 90% of patients with this syndrome have significant fixed atherosclerotic coronary artery disease. Other complex, interacting pathophysiological mechanisms may include coronary vasoconstriction, plaque rupture and thrombosis. Therapeutic strategies aim at either reduction of myocardial oxygen demand or restoration of coronary blood flow. Both alternatives have been suggested as treatment of choice. However, as long as the pathophysiological mechanism(s) is unknown in the individual case, the treatment will mainly be empirical or based on results from clinical trials of heterogeneous groups of patients with unstable angina with probably varying aetiology. The results from such studies indicate that some strategies may be of value, but others may even be harmful in treatment of patients with this unstable syndrome. In this situation nitrates seem to be a safe drug which may be used in most forms of irrespective of the underlying pathophysiological mechanism(s).

Angina Pectoris↗
PubMed1993

[The use of echocardiography in examining patients with unstable stenocardia].

The report presents the results of EchoCG study in 81 patients with unstable stenocardia admitted in 6-24 hours from the onslaught pain. With the help of EchoCG the myocardial contractile function was defined and the segmental kinetics of left ventricular wall was registered with respect to four variants of unstable stenocardia courses: stenocardia occurred for the first time, progressive stenocardia, variational stenocardia and postmyocardial infarction stenocardia. During the EchoCG examination at the moment of anginal attack the significant increase in left ventricular end-diastolic volume and end-systolic volume and decrease of total ejection fraction were noted. Also, not infrequently the zones of dyskinesia are recorded indicative of ischemia of these segments, which commonly have transient character. With the progress of myocardial ischemia the abnormalities of left ventricular diastolic fraction appear which are determined with the help of Doppler-EchoCG. Thus, the use of EchoCG in diagnostics of patients with unstable stenocardia allows more reliably to define the degree of myocardial changes.

Adult↗
PubMedDate not supplied

Nifedipine in the treatment of cardiovascular disease.

Nifedipine, a calcium channel blocking agent, has been shown safe and effective in the treatment of various cardiac disorders. In Prinzmetal's variant angina, nifedipine relieves the acute spasm of a large coronary artery, and thereby reverses the sudden decrease in myocardial oxygen supply. In chronic stable angina, the efficacy of nifedipine stems from an interplay of direct and reflex effects. A decrease in systemic vascular resistance, and thus, myocardial oxygen demand, is considered the most important effect. Although this is partially offset by baroreceptor-mediated reflex increases in blood pressure and heart rate, the net effect is a decrease in myocardial oxygen consumption. The importance of nifedipine-induced increases in coronary blood flow in relieving stable angina remains controversial. Numerous clinical trials in patients with chronic angina have demonstrated that nifedipine increases exercise tolerance by lowering the heart rate-blood pressure product (an approximation of myocardial oxygen consumption). The maximal double product during exercise, however, does not increase, suggesting that the drug does not importantly improve myocardial oxygen supply. Nifedipine may also be of value in the therapy of unstable angina, acute myocardial infarction, and hypertension, as well as in the protection of the myocardium at risk during open heart surgery. However, definite recommendations on the use of the drug for these indications must await results of ongoing randomized studies. The effects of nifedipine are dose-related. Larger doses have been shown more effective than smaller doses, as long as an appropriate blood pressure is maintained. The side effects of nifedipine are mild and related to its vasodilating action.

Angina Pectoris↗
PubMed1989

The role of calcium antagonists in the treatment of myocardial ischemia.

Calcium antagonists are often prescribed for treatment of ischemic heart disease. Therapeutic activity is achieved by reducing myocardial oxygen requirements and by increasing blood supply in ischemic heart disease associated with coronary artery spasms. The efficacy of calcium antagonists depends on the type and clinical presentation of ischemic heart disease: (1) in vasospastic angina (variant angina, short episodes of angina at rest), first-line therapy with calcium antagonists will reduce the number of ischemic episodes and improve long-term prognosis. (2) In effort angina the efficacy of calcium antagonists is comparable with that of beta blockers. (3) In unstable angina the use of calcium antagonists is controversial. Large-scale studies with nifedipine showed no benefit when it was given alone but an additive effect in patients pretreated with beta blockers. In contrast, diltiazem and verapamil appear to have comparable efficacy to beta blockers in patients with unstable angina. (4) After myocardial infarction the results of treatment with calcium antagonists have been disappointing. Nifedipine and verapamil did not reduce mortality or the incidence of reinfarction. In one study diltiazem significantly reduced the rate of reinfarction in patients who had had a non-Q wave infarction, but in a recent large-scale multicenter trial it had no effect on mortality and cardiac events in patients with evidence of both Q- and non-Q wave infarctions. Other secondary preventative measures against reinfarction, such as the use of beta-blockers and aspirin, appear to be more effective than calcium antagonists. The most frequently prescribed calcium antagonists, verapamil, diltiazem, and nifedipine, each of which represents a different chemical class, have in general similar efficacy in vasospastic and effort angina. Their different pharmacologic profile, such as the slowing of heart rate with verapamil or diltiazem and a more marked vasodilatation with nifedipine and other dihydropyridines, may become clinically relevant in individual patients. The new dihydropyridine derivatives have a pharmacologic profile comparable to that of nifedipine but some of these compounds, especially amlodipine, have more favorable pharmacokinetics, such as a prolonged elimination half-life. These agents may offer the advantage of a more practical dosage regimen for long-term treatment in patients with ischemic heart disease.

Angina Pectoris↗
PubMedDate not supplied

Ergonovine-induced constrictions of epicardial coronary arteries in conscious dogs: alpha-adrenoceptors are not involved.

The effect of i.v. ergonovine tartrate infusions (0.05-20 micrograms/kg/min, 12 minutes duration) on coronary arteries was studied in 14 conscious dogs instrumented to continuously measure vascular diameter by an ultrasonic dimension gauge using 10-MHz piezoelectric crystals. Ergonovine induced a biphasic coronary response: small, transient dilation during the first minutes of infusion, followed by slowly developing constriction reaching its maximum 5 to 15 minutes after the end of the infusion and persisting at this level for at least 10 minutes. The threshold dosage for significant constriction was 0.05 microgram/kg/min. A dosage of 5 micrograms/kg/min (cumulative 60 micrograms/kg, corresponding to 35 micrograms/kg ergonovine maleate) caused a decline in mean left circumflex artery diameter by 137 +/- 15 micrometers (= 4.6%) without significantly altering heart rate, plasma catecholamines or plasma renin activity. Coronary venous O2 saturation did not decline, indicating the absence of coronary resistance vessel constriction. The epicardial artery constriction was not attenuated by a vasopressin antagonist. Under adrenergic blockade (2 mg/kg phentolamine and 2 mg/kg nadolol) or under ganglionic blockade (5 mg/kg pentolinium tartrate), ergonovine (5 micrograms/kg /min) caused substantial elevation in mean arterial pressure, while the decline in coronary artery diameter was attenuated. When this increase in arterial pressure was prevented by appropriate bleeding, the ergonovine-induced coronary constriction was not diminished by adrenergic or ganglionic blockade. The serotonin antagonist methysergide (0.5 mg/kg) completely abolished the ergonovine-induced coronary artery vasomotion. It is concluded that ergonovine in dogs causes an epicardial coronary artery constriction comparable to the diffuse coronary artery narrowing in men not suffering from variant angina pectoris. These constrictions are not mediated by an adrenergic mechanism.

Adrenergic beta-Antagonists↗
PubMed1980

Refractory ergonovine-induced coronary vasospasm: importance of intracoronary nitroglycerin.

Recent experience has suggested that the ergonovine maleate test is a safe procedure for the diagnosis of variant angina pectoris, because ergonovine-induced coronary vasospasm has generally been reversible by sublingual nitroglycerin. This report describes five cases of ergonovine-induced coronary vasospasm that were refractory to sublingual nitroglycerin. Four of these patients had cardiac arrest. In two patients the vasospasm was responsive to intracoronary nitroglycerin administration. Three patients died as a reuslt of the test. The two survivors differed from the nonsurvivors in the total dose or ergonovine given (0.1 and 0.15 mg versus 0.17, 0.3 and 0.3 mg, respectively) and in the method of administration of ergonovine. The survivors were given serial doses of 0.05 mg each whereas the three nonsurvivors received either larger initial doses (0.1 followed by 0.07 mg) or progressive incremental doses (0.05, 0.1 and 0.15 mg serially). Sublingual nitroglycerin, given to all five patients, and intravenous nitroglycerin, given to three of the five, were ineffective in reversing vasospasm. Intracoronary nitroglycerin favorably altered the course of the survivors. Thus, the ergonovine maleate test is not benign and may cause severe coronary vasospasm that is unresponsive to sublingual and intravenous nitroglycerin, but may be reversed by intracoronary nitroglycerin.

Administration, Oral↗