**6.8 Side effects**

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

It is a short-acting dihydropyridine with a side effect profile similar to nifedipine; it has also been shown to be useful in angina. It is remarkably effective in

It is a second-generation dihydropyridine channel blocker of the nifedipine type. It is more selective for vascular smooth muscles than myocardial tissue. And it serves as an effective vasodilator. It is usually used in the treatment of angina and essential hypertension. Additionally, it exhibits a high degree of protein binding

It is a dihydropyridine calcium channel blocker that differs from other dihydropyridines as it dilates the cerebral blood vessels more than other dihydropyridines do. It is indicated in the treatment of subarachnoid hemorrhage-associated neuro-

It is a phenylalkylamine. It was introduced in 1962 as a coronary vasodilator. It is used for the treatment of angina pectoris, arrhythmias due to ischemic cardiac syndromes, and supraventricular arrhythmias as well. Verapamil's primary effect is on the slow Ca2+ channel, which results in a slowing of AV conduction and the sinus rate. It has a rapid absorption following oral administration. However, it is metabolized quickly and, therefore, has low bioavailability. Its main site of firstpass metabolism is the liver, forming several products. Yet, its metabolites have no significant biological effects. Verapamil has an elimination half-life of around 5 hours. Verapamil, like the dihydropyridines, causes little impact on venous return and preload but has more direct negative inotropic and chronotropic effects than the dihydropyridines at doses that produce arteriolar dilation and afterload reduction (**Figure 4**). Thus, the consequences of a reflex increase in adrenergic tone are generally offset by the direct cardio depressant effects of the drug. In patients without heart failure, oral administration of verapamil reduces peripheral vascular resistance and blood pressure with minimal changes in heart rate. Ventricular performance is not impaired and may improve, especially if ischemia limits performance. In contrast, in patients with heart failure, intravenous verapamil can cause a marked decrease in contractility and left ventricular function. The antianginal effect of verapamil, like that of all Ca2+ channel blockers, is due primarily to a

It was introduced in Japan as a cardiovascular agent for the treatment of angina pectoris. It was detected to dilate peripheral arteries and arterioles. By relieving coronary artery spasm, diltiazem increases myocardial oxygen supply, and by decreasing heart rate, it reduces myocardial oxygen demand. It is used in patients with variant angina as well. Additionally, it has electrophysiological properties similar to those of verapamil and, therefore, is used as an antiarrhythmic agent, but it is less potent than verapamil. It has a rapid oral absorption through the digestive tract, and it reaches peak plasma

**6.3 Nicardipine**

vasospastic angina.

and has a half-life ranging from 10 to 18 hours.

reduction in myocardial O2 demand [7].

**6.4 Felodipine**

**6.5 Nimodipine**

logical deficits.

**6.6 Verapamil**

**224**

**6.7 Diltiazem**

