Can you take Atorvastatin with Verapamil?

Atorvastatin has a major potential interaction with Alcoholism.

The use of most HMG-CoA reductase inhibitors is contraindicated in patients with active liver disease, decompensated cirrhosis, or unexplained persistent elevations of serum transaminases. HMG-CoA reductase inhibitors are extensively metabolized by the liver. Decreased drug metabolism may lead to accumulation and increased risk of toxicity, including biochemical abnormalities of liver function and, rarely, jaundice, hepatitis, cirrhosis, fatty change in the liver, and fulminant hepatic necrosis. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. A lower initial dosage may be appropriate, and clinical monitoring of liver transaminase levels according to the individual manufacturer product information is recommended. Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, consideration should be given to a reduction in dosage or withdrawal of therapy.

Verapamil has a major potential interaction with Aortic Stenosis.

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.

Verapamil has a major potential interaction with Cardiogenic Shock.

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.

Atorvastatin has a moderate potential interaction with Central Nervous System Disorders.

Cognitive impairment (e.g., memory loss, forgetfulness, amnesia, memory impairment, confusion) have been observed in patients receiving statins. The reports are usually not serious, and reversible upon statin discontinuation. Caution is recommended when using these agents in patients with cognitive impairment.

Atorvastatin has a moderate potential interaction with Diabetes Mellitus.

Increases in hemoglobin A1c and fasting serum glucose levels have been reported with the use of certain HMG-CoA reductase inhibitors. Caution should be exercised when using these agents in diabetic patients and close monitoring is recommended.

Verapamil has a moderate potential interaction with Gastrointestinal Obstruction.

The controlled-onset, extended-release formulation of verapamil (Covera-HS) contains a non-deformable material. There have been rare reports of obstructive symptoms in patients with known strictures following the ingestion of similar sustained-release products. Therapy with the controlled-onset, extended-release formulation of verapamil should be administered cautiously in patients with preexisting severe gastrointestinal narrowing or obstruction, whether pathologic or iatrogenic.

Verapamil has a major potential interaction with Heart Attack.

The use of verapamil is contraindicated 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, verapamil 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. Verapamil has a negative inotropic effect, which in most patients is compensated by a simultaneous reduction in afterload (i.e. decreased systemic vascular resistance) without a net impairment of ventricular performance. However, congestive heart failure or pulmonary edema have developed in approximately 2% of patients treated with verapamil. Mild symptoms of cardiac failure should be under control, if possible, prior to initiating verapamil therapy.

Verapamil has a major potential interaction with Heart Block.

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.

Verapamil has a major potential interaction with Heart Failure.

The use of verapamil is contraindicated 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, verapamil 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. Verapamil has a negative inotropic effect, which in most patients is compensated by a simultaneous reduction in afterload (i.e. decreased systemic vascular resistance) without a net impairment of ventricular performance. However, congestive heart failure or pulmonary edema have developed in approximately 2% of patients treated with verapamil. Mild symptoms of cardiac failure should be under control, if possible, prior to initiating verapamil therapy.

Verapamil has a major potential interaction with Hypertrophic Cardiomyopathy.

The use of verapamil in patients with hypertrophic cardiomyopathy, or idiopathic hypertrophic subaortic stenosis, has been associated with serious side effects such as pulmonary edema, severe hypotension, sinus bradycardia, AV block, sinus arrest, and death. However, a causal relationship has not been established. Therapy with verapamil should be administered cautiously in patients with hypertrophic cardiomyopathy. Dosage reduction or drug discontinuation may be required if severe adverse effects occur.

Verapamil has a major potential interaction with Hypotension.

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.

Verapamil has a major potential interaction with Ischemic Heart Disease.

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.

Atorvastatin has a major potential interaction with Liver Disease.

The use of most HMG-CoA reductase inhibitors is contraindicated in patients with active liver disease, decompensated cirrhosis, or unexplained persistent elevations of serum transaminases. HMG-CoA reductase inhibitors are extensively metabolized by the liver. Decreased drug metabolism may lead to accumulation and increased risk of toxicity, including biochemical abnormalities of liver function and, rarely, jaundice, hepatitis, cirrhosis, fatty change in the liver, and fulminant hepatic necrosis. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with a history of liver disease and/or heavy alcohol use. A lower initial dosage may be appropriate, and clinical monitoring of liver transaminase levels according to the individual manufacturer product information is recommended. Patients who develop elevated ALT or AST levels during therapy should be monitored until abnormalities resolve. If an increase above 3 times the upper limit of normal persists, consideration should be given to a reduction in dosage or withdrawal of therapy.

Verapamil has a major potential interaction with Liver Disease.

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.

Atorvastatin has a moderate potential interaction with Myoneural Disorder.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

Verapamil has a moderate potential interaction with Myoneural Disorder.

Verapamil has been reported to decrease neuromuscular transmission in patients with Duchenne's muscular dystrophy and to prolong recovery from the neuromuscular blocking agent, vecuronium. Therapy with verapamil should be administered cautiously in patients with attenuated neuromuscular transmission or myopathy, since these conditions may be exacerbated. A reduced dosage may be appropriate.

Atorvastatin has a moderate potential interaction with Myopathy.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

Verapamil has a moderate potential interaction with Myopathy.

Verapamil has been reported to decrease neuromuscular transmission in patients with Duchenne's muscular dystrophy and to prolong recovery from the neuromuscular blocking agent, vecuronium. Therapy with verapamil should be administered cautiously in patients with attenuated neuromuscular transmission or myopathy, since these conditions may be exacerbated. A reduced dosage may be appropriate.

Verapamil has a major potential interaction with Preexcitation Syndrome.

The use of verapamil 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). Intravenous verapamil has been reported to 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. Although these events have not been associated with chronic use of oral verapamil, a similar risk may exist.

Atorvastatin has a moderate potential interaction with Renal Dysfunction.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

Atorvastatin has a moderate potential interaction with Renal Dysfunction.

Some HMG-CoA reductase inhibitors (e.g., fluvastatin) have not been studied in patients with severe renal dysfunction or end-stage renal disease. Some others (e.g., pitavastatin, simvastatin) require a dose reduction when used in this group of patients. Caution and close monitoring are advised when using these drugs in patients with renal dysfunction.

Verapamil has a moderate potential interaction with Renal Dysfunction.

Approximately 70% of an administered dose of verapamil is excreted as metabolites in the urine. The primary metabolite, norverapamil, has about 20% the cardiovascular activity and can reach steady-state plasma concentrations approaching those of the parent drug. Patients with impaired renal function may be at greater risk for adverse effects due to drug and metabolite accumulation. Therapy with verapamil should be administered cautiously in such patients, with appropriate monitoring for excessive pharmacologic effects (e.g., abnormal prolongation of PR interval) and the dosage adjusted accordingly as necessary.

Verapamil has a major potential interaction with Sinus Node Dysfunction.

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.

Atorvastatin has a moderate potential interaction with Underactive Thyroid.

HMG-CoA reductase inhibitors may cause myopathy and rhabdomyolysis; acute renal failure secondary to myoglobinuria and rare fatalities have occurred due to rhabdomyolysis in patients treated with statins. The myopathy may be dose-related and is characterized by unexplained muscle weakness, pain, or tenderness accompanied by increases in creatine phosphokinase (CPK) values exceeding 10 times the upper limit of normal. Therapy with HMG-CoA reductase inhibitors should be administered cautiously in patients with preexisting myopathy, in those with predisposing factors for myopathy, or with a history of myoneural disorder, since it may delay the recognition or confound the diagnosis of a drug-induced musculoskeletal effect. Patients should be advised to report promptly any unusual muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Periodic CPK determinations may be considered in some patients, although the value of such monitoring is uncertain. HMG-CoA reductase inhibitor therapy should be withdrawn if markedly elevated CPK levels occur or if drug-related myopathy is diagnosed or suspected.

Verapamil has a major potential interaction with Ventricular Arrhythmia.

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.