Cartia XT Disease Interactions

The use of some calcium channel blockers (CCBs) is contraindicated in patients with advanced aortic stenosis. CCBs whose pharmacologic effect is partially dependent on their ability to reduce afterload (e.g., diltiazem, nicardipine, nifedipine, verapamil) may be of less benefit in these patients due to a fixed impedance to flow across the aortic valve and may, in fact, worsen rather than improve myocardial oxygen balance. Rarely, heart failure has developed following the initiation of these CCBs, particularly in patients receiving concomitant beta-blocker therapy.

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The use of some calcium channel blockers (CCBs) is contraindicated in patients with severe bradyarrhythmia, sick sinus syndrome (unless a functioning pacemaker is present), or heart block greater than the first degree (unless a functioning pacemaker is present). CCBs like bepridil, diltiazem and verapamil have a negative effect on AV conduction and the SA node and may exacerbate these conditions.

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In general, calcium channel blockers (CCBs) should not be used in patients with hypotension (systolic pressure < 90 mm Hg) or cardiogenic shock. Due to potential negative inotropic and peripheral vasodilating effects, the use of CCBs may further depress cardiac output and blood pressure, which can be detrimental in these patients. The use of verapamil and diltiazem is specifically contraindicated under these circumstances.

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Increased frequency, duration, and/or severity of angina, as well as acute myocardial infarction, have rarely developed during initiation or dosage increase of calcium channel blockers (CCBs), particularly in patients with severe obstructive coronary artery disease and those treated with immediate-release formulations. The mechanism of this effect is not established. Therapy with CCBs should be administered cautiously in patients with significant coronary artery disease.

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Calcium channel blockers (CCBs) are extensively metabolized by the liver. The half-lives of CCBs may be prolonged substantially in patients with severe hepatic impairment, with the potential for significant drug accumulation. In addition, the use of some CCBs has been associated with elevations in serum transaminases, both with and without concomitant elevations in alkaline phosphatase and bilirubin. While these effects may be transient and reversible, some patients have developed cholestasis or hepatocellular injury. Therapy with CCBs should be administered cautiously and often at reduced dosages in patients with significantly impaired hepatic function. Periodic monitoring of liver function is advised.

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Diltiazem has demonstrated a negative inotropic effect in isolated animal tissue preparations but rarely in clinical situations. Hemodynamic studies in humans with normal ventricular function and in patients with a compromised myocardium have not shown a reduction in cardiac index nor consistent negative effects on contractility. However, worsening of congestive heart failure has been reported in patients with preexisting impairment of ventricular function. Therapy with diltiazem should be administered cautiously, if at all, in patients with severe left ventricular dysfunction (e.g., ejection fraction < 30%) or moderate to severe symptoms of cardiac failure and in patients with any degree of ventricular dysfunction if they are receiving a beta-adrenergic blocker. Likewise, diltiazem should not be given to patients with acute myocardial infarction and pulmonary congestion documented by X-ray on admission, since associated heart failure may be acutely worsened. Mild symptoms of cardiac failure should be under control, if possible, prior to initiating diltiazem therapy.

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The use of intravenous diltiazem is contraindicated for the management of atrial flutter or fibrillation in patients with an accessory AV tract (e.g., those with Wolff-Parkinson-White or Lown-Ganong-Levine syndrome). Diltiazem can cause ventricular fibrillation and cardiac arrest in such patients, the mechanism of which is related to the drug's ability to shorten the refractory period and accelerate antegrade conduction within the accessory pathway.

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The use of intravenous diltiazem or verapamil is contraindicated in patients with ventricular tachycardia. IV administration of a calcium channel blocker can precipitate cardiac arrest in such patients. Marked hemodynamic deterioration and ventricular fibrillation have occurred in patients with wide-complex ventricular tachycardia (QRS >= 0.12 seconds) treated with IV verapamil.

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Diltiazem is extensively metabolized by the liver and subsequently excreted in the urine, primarily as metabolites. Limited data suggest that the pharmacokinetic disposition of diltiazem is not altered in the presence of renal insufficiency or even end-stage renal disease. However, the effects of possible metabolite accumulation have not been studied. The manufacturers recommend that therapy with diltiazem be administered cautiously in patients with impaired renal function. Laboratory parameters of renal function should be monitored at regular intervals.

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