Left ventricular consequences of renal transplantation and calcium-channel blockers

The calcium-channel blockers are useful in treating a variety of cardiovascular disorders. Due to their antiischemic and spasmolytic properties, these agents have been studied in the prophylaxis and treatment of acute myocardial infarction. This article reviews this application with respect to reduction of mortality, infarct size, and reinfarction rate. Of the agents currently available for clinical use, nifedipine has been studied most extensively. This agent shows no beneficial effects in this setting and its use may in fact be harmful. Of the few trials that have been conducted with verapamil, none have shown decreased mortality. Verapamil may reduce infarct size although further confirmation is required. Diltiazem is the only agent that has been shown to have short- and long-term benefits in the patient with acute myocardial infarction. Proper patient selection is of utmost importance in ensuring successful therapy. In particular, those patients with non-Q-wave infarctions and/or normal left ventricular function can be expected to derive the most benefit in terms of reducing mortality and reinfarction rate associated with the acute event.

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Prevalence and factors associated with left ventricular dysfunction in the EULAR Scleroderma Trial and Research group (EUSTAR) database of patients with systemic sclerosis

Annals of the Rheumatic Diseases ◽

10.1136/ard.2008.103382 ◽

2009 ◽

Vol 69 (01) ◽

pp. 218-221 ◽

Cited By ~ 139

Author(s):

Y Allanore ◽

C Meune ◽

M C Vonk ◽

P Airo ◽

E Hachulla ◽

...

Keyword(s):

Systemic Sclerosis ◽

Calcium Channel ◽

Multiple Regression ◽

Calcium Channel Blockers ◽

Left Ventricular ◽

Second Phase ◽

Channel Blockers ◽

Muscle Involvement ◽

Factors Associated ◽

Lv Dysfunction

Objectives:To measure the prevalence of, and factors associated with, left ventricular (LV) dysfunction in systemic sclerosis (SSc).Methods:The EUSTAR database was first searched. A case-control study of a patient subset was then performed to further identify independent factors associated with LV dysfunction by simple and multiple regression.Results:Of 7073 patients, 383 (5.4%) had an LV ejection fraction (EF) of <55%. By multiple regression analysis, age, sex, diffuse cutaneous disease, disease duration, digital ulcerations, renal and muscle involvement, disease activity score, pulmonary fibrosis and pulmonary arterial hypertension were associated with LV dysfunction. In the second phase, 129 patients with SSc with LVEF <55% were compared with 256 patients with SSc with normal LVEF. Male sex (OR 3.48; 95% CI 1.74 to 6.98), age (OR 1.03; 95% CI 1.01 to 1.06), digital ulcerations (OR 1.91; 95% CI 1.05 to 3.50), myositis (OR 2.88; 95% CI 1.15 to 7.19) and use of calcium channel blockers (OR 0.41; 95% CI 0.22 to 0.74) were independent factors associated with LV dysfunction.Conclusion:The prevalence of LV dysfunction in SSc is 5.4%. Age, male gender, digital ulcerations, myositis and lung involvement are independently associated with an increased prevalence of LV dysfunction. Conversely, the use of calcium channel blockers may be protective.

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Calcium-channel blockers for the prevention of stroke: from scientific evidences to the clinical practice

Italian Journal of Medicine ◽

10.4081/itjm.2008.1.37 ◽

2013 ◽

pp. 37-43

Author(s):

S. Taddei

Keyword(s):

Blood Pressure ◽

Cardiovascular Risk ◽

Calcium Channel ◽

Calcium Channel Blockers ◽

Ventricular Hypertrophy ◽

Blood Pressure Reduction ◽

Left Ventricular ◽

Channel Blockers ◽

Pressure Reduction ◽

Drug Classes

AIM OF THE REVIEW The present review aims to analyze the role of calcium-channel blockers, and particularly newer molecules, as first-line therapy for cerebrovascular disease. BACKGROUND Stroke is the leading cause of disability in the general population. Among traditional cardiovascular risk factors, hypertension has a key role in the genesis of both hemorrhagic and ischemic stroke and a direct correlation exists between blood pressure values and the risk of stroke. Moreover, blood pressure reduction has been demonstrated to be the most important route to reduce stroke incidence and recurrence. However, the mere reduction of blood pressure values does not normalize the cardiovascular risk of the hypertensive patient. It is therefore necessary to use drug classes that beyond their blood pressure-lowering effect have also an additional effect in terms of organ protection. Among these, calcium-channel blockers have a crucial profile. Firstly, they are effective in inducing left ventricular hypertrophy regression, with a strength at least equal to that of ACE-inhibitors. Secondly, they have an antithrombotic and an endothelium-protecting effect, mediated by their antioxidant activity. Finally, calcium-channel blockers are the most powerful drugs in preventing vascular remodeling. For these reasons this drug class has probably the strongest antiatherosclerotic effect, and it is the first-choice treatment mainly for cerebrovascular disease. Among different available calcium-channel blockers, the newer ones seem to possess pharmacokinetic characteristics allowing a more homogeneous 24 hours coverage as compared to older molecules, and preliminary data seem to suggest a greater beneficial effect also on left ventricular hypertrophy and lower incidence of side effects. CONCLUSIONS Although blood pressure reduction is the main tool to reduce cerebrovascular risk in hypertensive patients, some drug classes, such as calciumchannel blockers, seem to provide a protective action beyond the mere antihypertensive effect, and represent a key element in the prevention of atherosclerosis.

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Effect of calcium channel blockers on the incidence of myocardial infarction in patients with left ventricular dysfunction

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(96)80335-4 ◽

1996 ◽

Vol 27 (2) ◽

pp. 36

Author(s):

John B. Kostis ◽

Alan C. Wilson ◽

Nora M. Cosgrove ◽

Clifton R. Lacy

Keyword(s):

Myocardial Infarction ◽

Calcium Channel ◽

Left Ventricular Dysfunction ◽

Calcium Channel Blockers ◽

Ventricular Dysfunction ◽

Left Ventricular ◽

Channel Blockers

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Amlodipine inhibits granulation tissue cell apoptosis through reducing calcineurin activity to attenuate postinfarction cardiac remodeling

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00303.2007 ◽

2007 ◽

Vol 293 (4) ◽

pp. H2271-H2280 ◽

Cited By ~ 13

Author(s):

Atsushi Ogino ◽

Genzou Takemura ◽

Hiromitsu Kanamori ◽

Hideshi Okada ◽

Rumi Maruyama ◽

...

Keyword(s):

Myocardial Infarction ◽

Calcium Channel ◽

Granulation Tissue ◽

Calcium Channel Blockers ◽

Cardiac Remodeling ◽

Treated Group ◽

Left Ventricular ◽

Tissue Cell ◽

Channel Blockers ◽

Calcineurin Activity

Although amlodipine, a long-acting L-type calcium channel blocker, reportedly prevents left ventricular remodeling and dysfunction after myocardial infarction, the mechanism responsible is not yet well understood. Myocardial infarction was induced in mice by ligating the left coronary artery. Treatment of mice with amlodipine (10 mg·kg−1·day−1), beginning on the third day postinfarction, significantly improved survival and attenuated left ventricular dilatation and dysfunction 4 wk postinfarction compared with treatment with saline or hydralazine. Although infarct sizes did not differ among the groups, the infarcted wall thickness was greater and the infarct segment length was smaller in the amlodipine-treated group, and cellular components, including vessels and myofibroblasts, were abundant within the infarcted area. Ten days postinfarction (the subacute stage), the proliferation of granulation tissue cells in the infarcted area was similar among the groups, but the incidence of apoptosis was significantly lower in the amlodipine-treated group, where Bad, a proapoptotic Bcl-2 family protein, was significantly phosphorylated (inactivated). Calcineurin, which dephosphorylates (activates) Bad, was upregulated in infarcted hearts, but its levels were significantly reduced by amlodipine treatment. In vitro, Fas stimulation augmented calcineurin activity and induced apoptosis among infarct tissue-derived myofibroblasts; both of those effects were strongly inhibited by amlodipine, two other calcium channel blockers (verapamil or nifedipine), and two calcineurin inhibitors (cyclosporin A or FK-506). Amlodipine inhibits Fas-mediated granulation tissue cell apoptosis in infarcted hearts, possibly by attenuating the activities of calcineurin and Bad. These findings may provide new insight into the mechanism by which calcium channel blockers attenuate postinfarction cardiac remodeling and dysfunction.

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