Effects of nifedipine on myocardial perfusion during exercise in chronic stable angina pectoris

Rice, Kenneth A.; Gervino, Ernest V.; Jarisch, Wolfram; Stone, Peter H.

doi:10.1016/0002-9149(90)90320-z

Cited by 23 publications

(4 citation statements)

References 24 publications

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“…50 A reduction in ischemia on exercise treadmill tests, reduced ST-segment changes on ambulatory ECG monitoring, increased coronary artery blood flow, and improved ventricular dysfunction associated with ischemia were found with both agents. 51 –57 These results support the notion that CCBs are highly effective in reducing ischemic episodes in patients with vasospastic angina. 58 –60 However, there is little evidence showing that CCBs decrease the modulation of calcium sensitivity postulated by the increase in calcium sensitivity phenomenon.…”

Section: Pharmacotherapy Of Vasospastic Anginasupporting

confidence: 78%

Pharmacotherapy of Vasospastic Angina

Harris

Hale

Dasari

et al. 2016

J Cardiovasc Pharmacol Ther

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Vasospastic angina is a diagnosis of exclusion that manifests with signs and symptoms, which overlap with obstructive coronary artery disease, most often ST-segment elevation myocardial infarction. The pharmacotherapy that is available to treat vasospastic angina can help ameliorate angina symptoms. However, the etiology of vasospastic angina is ill-defined, making targeted pharmacotherapy difficult. Most patients receive pharmacotherapy that includes calcium channel blockers and/or long-acting nitrates. This article reviews the efficacy and safety of the pharmacotherapy used to treat vasospastic angina. High-dose calcium channel blockers possess the most evidence, with respect to decreasing angina incidence, frequency, and duration. However, not all patients respond to calcium channel blockers. Nitrates and/or alpha1-adrenergic receptor antagonists can be used in patients who respond poorly to calcium channel blockers. Albeit, evidence for use of nitrates and alpha1-adrenergic receptor antagonists in vasospastic angina is not as robust as calcium channel blockers and can exacerbate adverse effects when added to calcium channel blocker therapy. Despite having a clear benefit in patients with obstructive coronary artery disease, the benefit of beta-adrenergic receptor antagonists, statins, and aspirin remains unclear. More data are needed to elucidate whether or not these agents are beneficial or harmful to patients being treated for vasospastic angina. Overall, the use of pharmacotherapy for the treatment of vasospastic angina should be guided by patient-specific factors, such as tolerability, adverse effects, drug-drug, and drug-disease interactions.

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Section: Pharmacotherapy Of Vasospastic Anginasupporting

confidence: 78%

Pharmacotherapy of Vasospastic Angina

Harris

Hale

Dasari

et al. 2016

J Cardiovasc Pharmacol Ther

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“…A rise in coronary blood flow further contributes to correct myocardial oxygen imbalance. These drugs lower the frequency of angina, reduce the need for nitrates, extend treadmill walking time, and improve ischemic ST-segment changes on exercise testing and electrocardiographic monitoring 5,30–32. Amlodipine, in particular, may have some independent action in relieving diastolic dysfunction other than a reduction in BP 33…”

Section: Calcium Channel Blockersmentioning

confidence: 99%

Recent advances in the management of chronic stable angina II. Anti-ischemic therapy, options for refractory angina, risk factor reduction, and revascularization

Kones¹

2010

VHRM

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The objectives in treating angina are relief of pain and prevention of disease progression through risk reduction. Mechanisms, indications, clinical forms, doses, and side effects of the traditional antianginal agents – nitrates, β-blockers, and calcium channel blockers – are reviewed. A number of patients have contraindications or remain unrelieved from anginal discomfort with these drugs. Among newer alternatives, ranolazine, recently approved in the United States, indirectly prevents the intracellular calcium overload involved in cardiac ischemia and is a welcome addition to available treatments. None, however, are disease-modifying agents. Two options for refractory angina, enhanced external counterpulsation and spinal cord stimulation (SCS), are presented in detail. They are both well-studied and are effective means of treating at least some patients with this perplexing form of angina. Traditional modifiable risk factors for coronary artery disease (CAD) – smoking, hypertension, dyslipidemia, diabetes, and obesity – account for most of the population-attributable risk. Individual therapy of high-risk patients differs from population-wide efforts to prevent risk factors from appearing or reducing their severity, in order to lower the national burden of disease. Current American College of Cardiology/American Heart Association guidelines to lower risk in patients with chronic angina are reviewed. The Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial showed that in patients with stable angina, optimal medical therapy alone and percutaneous coronary intervention (PCI) with medical therapy were equal in preventing myocardial infarction and death. The integration of COURAGE results into current practice is discussed. For patients who are unstable, with very high risk, with left main coronary artery lesions, in whom medical therapy fails, and in those with acute coronary syndromes, PCI is indicated. Asymptomatic patients with CAD and those with stable angina may defer intervention without additional risk to see if they will improve on optimum medical therapy. For many patients, coronary artery bypass surgery offers the best opportunity for relieving angina, reducing the need for additional revascularization procedures and improving survival. Optimal medical therapy, percutaneous coronary intervention, and surgery are not competing therapies, but are complementary and form a continuum, each filling an important evidence-based need in modern comprehensive management.

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“…From multiple trials, CCBs decrease the frequency of angina, reduce the need for nitrates, extend treadmill walking time, and improve ischemic ST-segment changes on exercise testing and electrocardiographic monitoring (Gibbons et al, 2003;Heidenreich et al, 1999;Nissen et al, 2004;Rice et al, 1990). Amlodipine, in particular, may have some independent action in relieving diastolic dysfunction other than by a reduction in blood pressure (Tapp et al, 2010), potentially improving myocardial oxygen supply by enhancing perfusion pressure.…”

Section: Clinical Applicationmentioning

confidence: 99%