**7.3 Calcium channel blockers for stable angina**

All calcium channel blockers can be used in the treatment of stable angina pectoris. They vasodilate coronary arteries, reduce coronary resistance, increase coronary blood flow, and may enhance the development of coronary collaterals. The vasodilatation and increase in coronary artery blood flow result from the blockade of calcium influx as well as an increase in the levels of nitric oxide and bradykinin; therefore, the increase in coronary artery blood flow is a result of bradykinin/nitric oxide-dependent and bradykinin/nitric oxide-independent mechanisms. They elicit a strong reflex beta-adrenergic response, making any potential negative inotropic or chronotropic effect clinically insignificant. This adrenergic response often includes

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*Calcium Channel Blockers*

inotropic effect.

patients with HCM.

tachycardia.

a second-choice drug.

**7.7 Calcium channel blockers for migraine**

*DOI: http://dx.doi.org/10.5772/intechopen.90778*

a reflex tachycardia. Verapamil and diltiazem are useful in angina because they decrease myocardial oxygen demand by acting as a negative inotropic and chronotropic effect, by lowering the systemic blood pressure, and by lowering heart rate by blocking AV node (**Figure 6**). The use of short-acting dihydropyridines, such as nifedipine, can exacerbate ischemia due to reflex tachycardia, and therefore, it can be used as a monotherapy in this setting. Calcium channel blockers are used with combination therapy with beta-blockers, which can be more effective than either therapy alone. Amlodipine or felodipine could be considered before other calcium channel blockers, given their better side effect profiles when used in combination with beta-blockers. In stable angina patients with suspension of a vasoactive component, a trial of a calcium channel blocker can be added to beta blocker agents. Calcium channel blockers, particularly verapamil and diltiazem, should be used with caution in patients with left ventricular systolic dysfunction, such as those with an ejection fraction less than 40 percent or heart failure due to their negative

**7.4 Calcium channel blockers for acute coronary syndrome**

calcium channel-blocking agents that lower the heart rate [9, 10].

**7.5 Calcium channel blockers for hypertrophic cardiomyopathy (HCM)**

**7.6 Calcium channel blockers in the treatment of cardiac arrhythmias**

Verapamil improves left ventricular outflow obstruction and symptoms in

Calcium channel blockers (CCBs) are useful antiarrhythmic agents in the management of certain arrhythmias, primarily supraventricular tachyarrhythmias. Verapamil is the drug of choice to terminate idiopathic fascicular ventricular

Verapamil can be used in the prevention of migraine headaches but is considered

**7.8 Calcium channel blockers for aneurysmal subarachnoid hemorrhage**

spasm among patients with aneurysmal subarachnoid hemorrhage.

It is essential to review the cause behind intracranial arterial spasm, mechanisms, diagnostic tools, and management to understand the role of CCBs in vaso-

Vascular calcification is specific for arteries, which can involve all arteries, including the carotid artery and cerebral arteries. Intracranial arterial calcification (IAC) was first detected in the early 1960s. It is associated with atherosclerosis, especially in older people. Vascular calcification is an integral part of the active process of atherosclerosis, occurring in up to 90% of atherosclerotic lesions. Recent clinical studies have consistently found the intracranial internal carotid artery (IICA) to be the most common site of IAC. The incidence of IICA calcification has been reported

Calcium channel blockers have been effective in reducing ischemia in patients with NSTE-ACS and persistent ischemia despite treatment with full-dose nitrates and beta-blockers as well as in patients with contraindications to beta-blockers and among those with hypertension. Such patients should receive non-dihydropyridine

**Figure 6.** *Sites of effects of calcium channel blockers in angina.*

### *Calcium Channel Blockers DOI: http://dx.doi.org/10.5772/intechopen.90778*

*New Insight into Cerebrovascular Diseases - An Updated Comprehensive Review*

myocardial infarct-free survival in vasospastic angina patients.

All calcium channel blockers can be used in the treatment of stable angina pectoris. They vasodilate coronary arteries, reduce coronary resistance, increase coronary blood flow, and may enhance the development of coronary collaterals. The vasodilatation and increase in coronary artery blood flow result from the blockade of calcium influx as well as an increase in the levels of nitric oxide and bradykinin; therefore, the increase in coronary artery blood flow is a result of bradykinin/nitric oxide-dependent and bradykinin/nitric oxide-independent mechanisms. They elicit a strong reflex beta-adrenergic response, making any potential negative inotropic or chronotropic effect clinically insignificant. This adrenergic response often includes

**7.3 Calcium channel blockers for stable angina**

stenosis. Variant angina results from reduced blood flow (a consequence of transient localized vasoconstriction) rather than increased O2 demand. Drug-induced causes (e.g., cocaine, amphetamines, sumatriptan, and related antimigraine drugs) should be excluded. CCBs are effective in about 90% of patients. These agents are considered first-line treatment and may be combined with nitrate. The effects of pharmacologic vasodilators on coronary flow reflect direct actions on vascular smooth muscle as well as secondary adjustments in resistance artery tone. All calcium channel blockers induce vascular smooth muscle relaxation and are to various degrees pharmacologic coronary vasodilators (**Figure 6**). In epicardial arteries, the vasodilator response is like nitroglycerin and is effective in preventing coronary vasospasm superimposed on coronary stenosis as well as in normal arteries of patients with variant angina. They also submaximally vasodilate coronary resistance vessels. In this regard, dihydropyridine derivatives such as nifedipine are particularly potent and can sometimes precipitate subendocardial ischemia in the presence of critical stenosis. This arises from a transmural redistribution of blood flow (coronary steal) as well as the tachycardia and hypotension that transiently occur with short half-life formulations of nifedipine. One study demonstrated that the use of calcium channel blocker therapy was an independent predictor of

**226**

**Figure 6.**

*Sites of effects of calcium channel blockers in angina.*

a reflex tachycardia. Verapamil and diltiazem are useful in angina because they decrease myocardial oxygen demand by acting as a negative inotropic and chronotropic effect, by lowering the systemic blood pressure, and by lowering heart rate by blocking AV node (**Figure 6**). The use of short-acting dihydropyridines, such as nifedipine, can exacerbate ischemia due to reflex tachycardia, and therefore, it can be used as a monotherapy in this setting. Calcium channel blockers are used with combination therapy with beta-blockers, which can be more effective than either therapy alone. Amlodipine or felodipine could be considered before other calcium channel blockers, given their better side effect profiles when used in combination with beta-blockers. In stable angina patients with suspension of a vasoactive component, a trial of a calcium channel blocker can be added to beta blocker agents. Calcium channel blockers, particularly verapamil and diltiazem, should be used with caution in patients with left ventricular systolic dysfunction, such as those with an ejection fraction less than 40 percent or heart failure due to their negative inotropic effect.
