Calcium Channel Blocking Agents in the Treatment of Cardiovascular Disorders. Part I: Basic and Clinical Electrophysiologic Effects

Antman, Elliott M.

doi:10.7326/0003-4819-93-6-875

Cited by 313 publications

(47 citation statements)

References 100 publications

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“…By comparison, little is known about the Ca channel (Hagiwara & Byerly, 1981;McDonald, 1982), and it will be interesting to see whether further studies with Ca channel blockers narrow this gap. On the clinical side, Ca channel blocking agents have become increasingly important in the treatment of cardiac and vascular disorders (Antman, Stone, Muller & Braunwald, 1980). It is almost certain that membrane potential and the frequency of Ca channel opening are key elements in the pharmacology of these drugs.…”

Section: Conclu8ionsmentioning

confidence: 99%

Cat ventricular muscle treated with D600: characteristics of calcium channel block and unblock.

McDonald¹,

Pelzer²,

Trautwein³

1984

The Journal of Physiology

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3. The time course of unblock was usually monoexponential. The time constant was voltage dependent and declined from 9 min at -50 mV to 5 s at -110 mV.4. Block appears to depend on channel state, resting channels being highly resistant to block and open channels very susceptible. D600 also binds to inactivated channels but at a much slower rate than to open channels. 5. A small U-shaped component of block was induced by conditioning to potentials between + 10 and + 80 mV. This block seemed to be unrelated to channel state, suggesting that drug binding may also be dependent on voltage.6. Quicker rates of block after repetitive conditioning, and slow wash-out of the drug, may indicate the existence of an intramembrane drug pool distinct from the primary pool in the intracellular fluid.7. The interaction of D600 with Ca channels is discussed in terms of a channel state model. In many respects this interaction resembles that of local anaesthetics with Na channels.

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Section: Conclu8ionsmentioning

confidence: 99%

Cat ventricular muscle treated with D600: characteristics of calcium channel block and unblock.

McDonald¹,

Pelzer²,

Trautwein³

1984

The Journal of Physiology

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“…Other studies have demonstrated that rapid depolarizations result in increased cytosolic Ca 2þ concentration (calcium overload) and ERP shortening in cardiac myocytes 4,[16][17][18][19] via changes in I CaL , I To and I Na and that inhibition of I Na results in decreased conduction velocity. Further, Balana et al reported that chronic AF was associated with down-regulated IK ATP currents, 8) and Brundel et al reported that mRNA levels of Kir6.2, which encodes for a portion of the IK ATP protein, are reduced in patients with 7) They also demonstrated that the reduction in levels of Kv4.3, Kv1.5 and Kv3.1, which encode for portions of the I To , IK ur and IK Ach proteins, could be reversed by maintenance of sinus rhythm.…”

Section: Atrial Refractorinessmentioning

confidence: 99%

Electrical Remodeling in Persistent Atrial Fibrillation May Be Mediated by Changes in the IKATP Channel

et al. 2005

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The goal of this study was to measure the effective refractory period (ERP), the conduction velocity (CV) and the wavelength (WL) after cardioversion in patients with persistent atrial fibrillation (AF) and to determine the effects of the adenosine triphosphate sensitive potassium channel (K ATP ) opening agent, nicorandil, on those parameters in patients with persistent AF.METHODS: Patients with AF underwent elective cardioversion followed by measurement of ERP and CV before and after administration of nicorandil. Parameters were measured again one week later, and the ERP and the CV was used to calculate WL.RESULTS: ERP was significantly shorter immediately after termination of AF than at the 1-week time point (193.4 vs. 228.7 msec p < 0:01). While there was no significant difference in ERP immediately after termination of AF when comparing measurements taken before and after the administration of nicorandil, ERP at the 1-week time point was shorter after nicorandil administration than before nicorandil administration (193.4 vs. 191.4 msec, n.s.; 228.7 vs. 217.2 msec, p < 0:01). Further, WL was higher at the 1-week time point after nicorandil administration than before nicorandil administration.CONCLUSIONS: These data indicate that the electrical remodeling that occurs after cardioversion is at least partially mediated by changes in K ATP channel behavior. Further, the electrophysiologic properties, that is, nicorandil prolonging the WL, may be of benefit in reducing the recurrence rate of AF. (J Arrhythmia 2005; 21: 371-377)

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“…Until the results of this trial become available and are widely disseminated to the practicing physician, it will be difficult to credit beta-blocking drugs with a major role in the decline in cardiovascular mortality. Similarly, while the new calcium channel antagonists, verapamil and nifedipine, appear to hold great promise for the treatment of coronary vasospasm and myocardial ischemia 24 in the United States, they have not yet been approved by the Federal Drug Administration (FDA). They remain investigational and are not readily available for physician use.…”

Section: New Drugs Surgical and Diagnostic Techniquesmentioning

confidence: 99%

Declining mortality in coronary heart disease.

Levy¹

1981

Arteriosclerosis

108

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Since 1968, there has been a dramatic, unprecedented decline in mortality from cardiovascular disease In the United States, especially from coronary heart disease and stroke. The decline has now been confirmed as real and has been observed In all age, sex, and race groups. Possible causes of the decline In coronary heart disease mortality Include the development of the concept of acute coronary care, new drugs, sophisticated surgical techniques such as coronary artery bypass, nonlnvaslve diagnostic methods for earlier disease detection, and the Identification of specific cardiovascular risk factors. The decline has been temporally related to risk factor awareness and modification (cigarette smoking cessation, hypertension control, diet change, and reduction In cholesterol). Thus, both primary prevention through lifestyle changes and Improved treatment regimes have played a role In the decline. (Arteriosclerosis 1:312-325, September/October 1981) I t is impossible to overemphasize the magnitude of the health care problem each year caused by coronary heart disease (CHD), which is the leading cause of death in the United States. All forms of cancer combined (the second leading cause of death) were responsible for nearly 400,000 deaths in the United States in 1978. In contrast, CHD alone was responsible for nearly 650,000 deaths in 1978 (figure 1), and over 150,000 of these occurred before age 65.1 Nearly one-third of the deaths from all causes in persons aged 35-64 years were due to CHD, and nearly 40% of all deaths in white males aged 55 and over were caused by CHD. In 1979 there were 4 million Americans with symptomatic CHD (nearly half below age 65). It is estimated that over 1.25 million Americans suffer a heart attack each year during which time 20% to 25% do not live long enough to receive definitive medical care.

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Calcium Channel Blocking Agents in the Treatment of Cardiovascular Disorders. Part I: Basic and Clinical Electrophysiologic Effects

Cited by 313 publications

References 100 publications

Cat ventricular muscle treated with D600: characteristics of calcium channel block and unblock.

Cat ventricular muscle treated with D600: characteristics of calcium channel block and unblock.

Electrical Remodeling in Persistent Atrial Fibrillation May Be Mediated by Changes in the IKATP Channel

Declining mortality in coronary heart disease.

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