Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Angina Pectoris, Variant”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources
PubMed1985

Transient myocardial ischemia with minimal electrocardiographic changes: an echocardiographic study in patients with Prinzmetal's angina.

Kn patients with Prinzmetal's angina, episodes of transient T wave abnormalities (T abn) are often documented in addition to the typical episodes of ST segment elevation (ST). As the interpretation of these minor ECG changes is still uncertain, we investigated if transient T abn are associated with reversible ventricular asynergies, similar to episodes with ST. For this purpose an ECG lead and a two-dimensional echocardiographic projection, which showed clear-cut changes during previous episodes of ST, were simultaneously monitored in five patients with Prinzmetal's angina for a total of 13 hours and 20 minutes. In all patients, the 30 episodes of ST recorded were all accompanied by reversible ventricular asynergies. Furthermore, in four of these patients, 14 episodes of T abn (peaking, flattening, or the appearance of a diphasic T wave) were recorded. All T abn were associated with reversible asynergies, as detected by three independent observers. The mechanical impairment occurred in the same ventricular wall both during ST and during T abn. During T abn the degree of mechanical impairment appeared less severe (hypokinesia in 12 and akinesia in two episodes) than during ST (hypokinesia in one, akinesia in 25, and dyskinesia in four episodes) (p less than 0.001). The duration of asynergies was less during T abn (107 +/- 76 seconds) than during ST (169 +/- 83 seconds) (p less than 0.05). Chest pain was reported in 5 of 14 episodes of T abn (36%) and in 20 of 30 (66%) episodes of ST (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Long-term prognosis of medically treated patients with vasospastic angina and no fixed significant coronary atherosclerosis.

The clinical course of 48 consecutive patients with vasospastic angina and minor coronary atherosclerosis (no stenoses greater than 50%) was analyzed during an average follow-up period of 47 months. The study group consisted of 37 men and 11 women. Patients were treated with usual doses of calcium antagonists. One patient died (2%) and three had myocardial infarctions (6%). Seventy-one percent were asymptomatic or had infrequent angina; 13% had recurrences but had periods of remission lasting at least 10 months. Only 16% had persistent angina. None of the clinical or angiographic findings at the time of diagnosis were predictive of myocardial infarction or death, and they could not separate angina-free patients from those with recurrences. Thus, vasospastic angina without fixed coronary narrowing has a good prognosis despite the possibility of recurrences. However, there is a slight risk of myocardial infarction and death. This fact should be considered if there are plans to discontinue treatment.

Adult↗
PubMed1989

Different coronary vasomotor effects of nifedipine and therapeutic correlates in angina with spontaneous and effort components versus Prinzmetal angina.

Flow impedance, probably of vasomotor origin, superimposed on severe coronary stenosis has been considered a trigger for the spontaneous component of angina occurring both on effort and at rest. To investigate more thoroughly this pathophysiologic aspect we evaluated (by means of quantitative coronary angiography) the acute vasomotor reaction to nifedipine (10 mg sublingually) of significant (greater than 50%) stenotic lesions in 22 patients with double-component angina. We also correlated this reaction with the clinical response (daily number of ischemic episodes evaluated by means of 48-hour Holter ambulatory monitoring) to treatment with nifedipine (20 mg four times a day); calcium channel blockade, in fact, is considered a specific remedy in cases of altered coronary vasomotility. Patients with Prinzmetal angina, who were known to have homogeneous coronary vasodilating reactions and favorable clinical responses to nifedipine, were studied by means of the same methods and served as the control group (14 patients). In double-component angina the residual lumen diameter of significant lesions was unchanged in two patients, enhanced in 10, and reduced in 10 after sublingual nifedipine; lumen variations from baseline values ranged from +1.29 to -1.56 mm. Acute changes in stenosis correlated closely with results obtained with oral treatment. In the group with Prinzmetal angina, coronary stenoses invariably responded with dilatation (the residual coronary lumen increased by an average of 69% of baseline); 100% of the patients in this group responded favorably to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

The efficacy of amlodipine in myocardial ischemia.

Calcium antagonists are among the most potent and efficacious drugs used in the treatment of angina pectoris. Amlodipine, a new member of this family of dihydropyridines, has a unique pharmacokinetic profile with high bioavailability and an extended period of pharmacodynamic activity. In formal randomized, double-blind, placebo-controlled trials with exercise tests carried out 24 hours after administration, amlodipine was significantly more effective than the placebo and comparable in efficacy with the calcium antagonist diltiazem and the beta-blocking drug nadolol. In addition to extending exercise capacity in patients with angina pectoris, amlodipine significantly reduces ECG evidence of myocardial ischemia. Amlodipine has also been found to be effective in reducing the anginal attack rate in patients with vasospastic angina. From the evidence available, it is concluded that once-daily treatment with amlodipine in the dose range of 5 to 10 mg is effective in improving exercise capacity and reducing anginal attack rate in patients with chronic stable angina pectoris and also those with vasospastic angina.

Adrenergic beta-Antagonists↗
PubMed1992

The effect of ergonovine on coronary vasodilatory reserve in patients with angiographically normal coronary arteries.

Ergonovine produces physiologic coronary artery narrowing in many patients without focal coronary spasm. The effect of ergonovine-induced coronary vasoconstriction on coronary vasodilatory reserve is unknown. Therefore we studied 10 patients with atypical chest pain and angiographically normal coronary arteries. The heart rate and blood pressure were recorded continuously and coronary Doppler flow velocity was measured continuously with a 20 MHz Doppler-tipped catheter. Ergonovine caused diffuse narrowing of the vessels in all patients, with a 12% +/- 5% change in diameter of the left anterior descending coronary artery (p less than 0.001). There was a significant change in systolic (17% +/- 12% change; p less than 0.05) and mean arterial pressure (13% +/- 13% change; p less than 0.05), with no significant change in mean coronary flow velocity with ergonovine. Ergonovine also did not attenuate the maximal hyperemic response with papaverine. Thus despite an increase in myocardial demand and a decrease in caliber of conductance coronary vessels, the coronary autoregulatory flow responses were intact after the administration of ergonovine.

Angina Pectoris, Variant↗
PubMed1992

Circadian fluctuations of tissue plasminogen activator antigen and plasminogen activator inhibitor-1 antigens in vasospastic angina.

To elucidate the circadian variation of fibrinolytic components in vasospastic angina, plasma levels of tissue plasminogen activator antigen (t-PA), free plasminogen activator inhibitor antigen (free PAI-1), t-PA/PAI-1 complex, and total PAI-1 were measured in venous plasma samples. Samples were taken every 6 hours (6:00 AM, noon, 6:00 PM, and midnight) for 24 hours in 14 patients with vasospastic angina, in 9 patients with exertional angina, and in 19 normal subjects. Twenty-four-hour Holter monitoring (Holter monitor, Del Mar Avionics, Irvine, Calif.) was also carried out in all subjects. All of the fibrinolytic components showed circadian variation, with a peak level at 6:00 AM in every study group except for the t-PA/PAI-1 complex in the group of patients with exertional angina. The values for all or the fibrinolytic components at each sampling time were higher in patients with coronary artery disease than in normal subjects. In particular, the mean value of free PAI-1 at 6:00 AM in patients with vasospastic angina was significantly higher than that in normal subjects and that in patients with exertional angina. This value of free PAI-1 in patients with vasospastic angina was closely associated with the duration of ischemic attacks. These results suggested that the circadian fluctuation of fibrinolytic components may be an important factor that leads to coronary thrombosis at the time of coronary spasm, especially in the early morning.

Acetylcholine↗
PubMed1994

Investigation of therapeutic mechanisms of atenolol and diltiazem in patients with variable-threshold angina.

The effects of beta-adrenoreceptor and calcium channel-blocking agents on the balance of myocardial oxygen supply and demand were studied in 15 patients (2 women and 13 men), aged 46 to 69 (mean 62) years, with variable-threshold angina. An exercise test was performed before therapy was begun, and 24-hour ambulatory ECG monitoring was performed after 1 week of long-acting nitrate therapy, in the third week after random assignment to either atenolol or diltiazem, and in the third week after crossover. All exercise tests were positive except in one patient taking diltiazem. The exercise time to 0.1 mV ST change was 4.2 +/- 1.7 minutes with no therapy, 5.1 +/- 1.6 minutes with nitrates, 6.6 +/- 0.8 minutes with diltiazem, and 6.5 +/- 2.1 minutes with atenolol. The rate-pressure product at 0.1 mV ST change was 20.9 +/- 4.6 with no therapy and 21.2 +/- 5.7 and 22 +/- 4.6 with nitrates and diltiazem, respectively, but fell to 15 +/- 3.9 beats.min.-1 mm Hg 10(-3) after atenolol (p < 0.01). There was no significant difference in the number of anginal attacks or in nitroglycerin consumption per week. The heart rate at the onset of ST-segment change during the exercise test and during ambulatory ECG monitoring was significantly lower during atenolol than during diltiazem treatment. Both atenolol and diltiazem were of similar efficacy in increasing nonischemic exercise duration in patients with variable-threshold angina and acted primarily by slowing the resting heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1977

Provocation of coronary spasm with ergonovine maleate. New test with results in 57 patients undergoing coronary arteriography.

Ergonovine maleate (Ergotrate) was given to 57 patients undergoing coronary arteriography for investigation of angina occurring at rest or without provocation when routine study showed normal arteries or insufficient occlusive disease to explain their symptoms. This provocative test induced coronary arterial spasm in 13 patients, 10 of whom had definite Prinzmetal's angina. The spasm was easily reversed with sublingually administered nitroglycerin. The spasm was occlusive or nearly occlusive in nine patients, and there was associated reproduction of the chest pain and S-T elevation similar to the spontaneous episodes. One patient with Prinzmetal's angina had S-T depression rather than elevation in association with the chest pain. The other three patients without Prinzmetal's angina had focal narrowing without coronary occlusion, reproduction of the chest pain or electrocardiographic changes. Of the 44 patients who did not demonstrate coronary spasm in response to ergonovine, 29 had normal coronary arteries and 15 had various degrees of atherosclerotic occlusive disease. We conclude that cautious administration of ergonovine maleate during coronary arteriography can be safely used to elicit coronary spasm in some patients who have insufficient fixed occlusive disease to explain their symptoms.

Adult↗