Drug Interactions between Betapace and Lipitor

Grapefruit juice can increase the blood levels of atorvastatin. This can increase the risk of side effects such as liver damage and a rare but serious condition called rhabdomyolysis that involves the breakdown of skeletal muscle tissue. In some cases, rhabdomyolysis can cause kidney damage and even death. You should limit your consumption of grapefruit juice to no more than 1 quart per day during treatment with atorvastatin. Let your doctor know immediately if you have unexplained muscle pain, tenderness, or weakness during treatment, especially if these symptoms are accompanied by fever or dark colored urine. You should also seek immediate medical attention if you develop fever, chills, joint pain or swelling, unusual bleeding or bruising, skin rash, itching, loss of appetite, fatigue, nausea, vomiting, dark colored urine, and/or yellowing of the skin or eyes, as these may be signs and symptoms of liver damage. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

Sotalol and ethanol (alcohol) may have additive effects in lowering your blood pressure. You may experience headache, dizziness, lightheadedness, fainting, and/or changes in pulse or heart rate. These side effects are most likely to be seen at the beginning of treatment, following a dose increase, or when treatment is restarted after an interruption. Let your doctor know if you develop these symptoms and they do not go away after a few days or they become troublesome. Avoid driving or operating hazardous machinery until you know how the medications affect you, and use caution when getting up from a sitting or lying position. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

Using sotalol together with multivitamin with minerals may decrease the effects of sotalol. Separate the administration times of sotalol and multivitamin with minerals by at least 2 hours. If your doctor does prescribe these medications together, you may need a dose adjustment or special test to safely use both medications. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor.

The use of sotalol is contraindicated in patients with congenital or acquired QT interval prolongation syndromes. Sotalol has dose-dependent proarrhythmic effects related to prolongation of the QT interval. The risk of torsades de pointes is progressively increased as the degree of prolongation becomes greater. The manufacturer states that sotalol should be used with particular caution in patients whose QTc is greater than 500 msec on- therapy. Serious consideration should be given to reducing the dosage or discontinuing therapy when the QTc exceeds 550 msec.

The use of sotalol is contraindicated in patients with hypokalemia (< 4 meq/L). Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of sotalol on the QT interval and should be corrected prior to institution of sotalol therapy. In addition, patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with sotalol.

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.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) in patients with a history of allergic reactions or anaphylaxis may be associated with heightened reactivity to culprit allergens. The frequency and/or severity of attacks may be increased during beta-blocker therapy. In addition, these patients may be refractory to the usual doses of epinephrine used to treat acute hypersensitivity reactions and may require a beta-agonist such as isoproterenol.

Some beta-adrenergic receptor blocking agents (i.e., non-cardioselective beta-blockers) are contraindicated in patients with bronchial asthma or with a history of bronchial asthma, or severe chronic obstructive pulmonary disease. In general, beta-adrenergic receptor blocking agents should not be used in patients with bronchospastic diseases. Beta blockade may adversely affect pulmonary function by counteracting the bronchodilation produced by catecholamine stimulation of beta-2 receptors. If beta-blocker therapy is necessary in these patients, an agent with beta-1 selectivity (e.g., atenolol, metoprolol, betaxolol) is considered safer, but should be used with caution nonetheless. Cardioselectivity is not absolute and can be lost with larger doses.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.

Some beta-adrenergic receptor blocking agents (i.e., non-cardioselective beta-blockers) are contraindicated in patients with bronchial asthma or with a history of bronchial asthma, or severe chronic obstructive pulmonary disease. In general, beta-adrenergic receptor blocking agents should not be used in patients with bronchospastic diseases. Beta blockade may adversely affect pulmonary function by counteracting the bronchodilation produced by catecholamine stimulation of beta-2 receptors. If beta-blocker therapy is necessary in these patients, an agent with beta-1 selectivity (e.g., atenolol, metoprolol, betaxolol) is considered safer, but should be used with caution nonetheless. Cardioselectivity is not absolute and can be lost with larger doses.

Beta-adrenergic receptor blocking agents (aka beta-blockers) in general should not be used in patients with overt congestive heart failure (CHF). Sympathetic stimulation may be important in maintaining the hemodynamic function in these patients, thus beta-blockade can worsen the heart failure. However, therapy with beta-blockers may be beneficial and can be administered cautiously in some CHF patients provided they are well compensated and receiving digitalis, diuretics, an ACE inhibitor, and/or nitrates. Carvedilol, specifically, is indicated for use with these agents in the treatment of mild to severe heart failure of ischemic or cardiomyopathic origin. There is also increasing evidence that the addition of a beta-blocker to standard therapy can improve morbidity and mortality in patients with advanced heart failure, although it is uncertain whether effectiveness varies significantly with the different agents. Data from one meta-analysis study suggest a greater reduction of mortality risk for nonselective beta-blockers than for beta-1 selective agents.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may mask symptoms of hypoglycemia such as tremors, tachycardia and blood pressure changes. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may inhibit catecholamine-mediated glycogenolysis, thereby potentiating insulin-induced hypoglycemia and delaying the recovery of normal blood glucose levels. Since cardioselectivity is not absolute, larger doses of beta-1 selective agents may demonstrate these effects as well. Therapy with beta-blockers should be administered cautiously in patients with diabetes or predisposed to spontaneous hypoglycemia.

The use of sotalol is contraindicated in patients with congenital or acquired QT interval prolongation syndromes. Sotalol has dose-dependent proarrhythmic effects related to prolongation of the QT interval. The risk of torsades de pointes is progressively increased as the degree of prolongation becomes greater. The manufacturer states that sotalol should be used with particular caution in patients whose QTc is greater than 500 msec on- therapy. Serious consideration should be given to reducing the dosage or discontinuing therapy when the QTc exceeds 550 msec.

The use of sotalol is contraindicated in patients with hypokalemia (< 4 meq/L). Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of sotalol on the QT interval and should be corrected prior to institution of sotalol therapy. In addition, patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with sotalol.

The use of sotalol is contraindicated in patients with congenital or acquired QT interval prolongation syndromes. Sotalol has dose-dependent proarrhythmic effects related to prolongation of the QT interval. The risk of torsades de pointes is progressively increased as the degree of prolongation becomes greater. The manufacturer states that sotalol should be used with particular caution in patients whose QTc is greater than 500 msec on- therapy. Serious consideration should be given to reducing the dosage or discontinuing therapy when the QTc exceeds 550 msec.

The use of sotalol is contraindicated in patients with hypokalemia (< 4 meq/L). Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of sotalol on the QT interval and should be corrected prior to institution of sotalol therapy. In addition, patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with sotalol.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.

Therapy with sotalol should be administered cautiously in patients with renal failure undergoing hemodialysis. The half-life of sotalol is prolonged (up to 69 hours) in anuric patients. Although sotalol is partially removed by hemodialysis, a rebound in drug concentration often occurs after dialysis is complete. Sotalol should preferably be administered after dialysis and after hemodynamic stability has been established. Heart rate and ECG, particularly the QTc interval, must be closely monitored.

The use of sotalol is contraindicated in patients with congenital or acquired QT interval prolongation syndromes. Sotalol has dose-dependent proarrhythmic effects related to prolongation of the QT interval. The risk of torsades de pointes is progressively increased as the degree of prolongation becomes greater. The manufacturer states that sotalol should be used with particular caution in patients whose QTc is greater than 500 msec on- therapy. Serious consideration should be given to reducing the dosage or discontinuing therapy when the QTc exceeds 550 msec.

The use of sotalol is contraindicated in patients with hypokalemia (< 4 meq/L). Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of sotalol on the QT interval and should be corrected prior to institution of sotalol therapy. In addition, patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with sotalol.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with hypotension or cardiogenic shock. Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to further depress cardiac output and blood pressure, which can be detrimental in these patients.

Heightened sensitivity to catecholamines may occur after prolonged use of beta-adrenergic receptor blocking agents (aka beta-blockers). Exacerbation of angina, myocardial infarction and ventricular arrhythmias have been reported in patients with coronary artery disease following abrupt withdrawal of therapy. Cessation of beta-blocker therapy, whenever necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks in patients with coronary insufficiency. Patients should be advised not to discontinue treatment without first consulting with the physician. In patients who experience an exacerbation of angina following discontinuation of beta-blocker therapy, the medication should generally be reinstituted, at least temporarily, along with other clinically appropriate measures.

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.

The use of sotalol is contraindicated in patients with congenital or acquired QT interval prolongation syndromes. Sotalol has dose-dependent proarrhythmic effects related to prolongation of the QT interval. The risk of torsades de pointes is progressively increased as the degree of prolongation becomes greater. The manufacturer states that sotalol should be used with particular caution in patients whose QTc is greater than 500 msec on- therapy. Serious consideration should be given to reducing the dosage or discontinuing therapy when the QTc exceeds 550 msec.

The use of sotalol is contraindicated in patients with hypokalemia (< 4 meq/L). Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of sotalol on the QT interval and should be corrected prior to institution of sotalol therapy. In addition, patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with sotalol.

The use of sotalol is contraindicated in patients with congenital or acquired QT interval prolongation syndromes. Sotalol has dose-dependent proarrhythmic effects related to prolongation of the QT interval. The risk of torsades de pointes is progressively increased as the degree of prolongation becomes greater. The manufacturer states that sotalol should be used with particular caution in patients whose QTc is greater than 500 msec on- therapy. Serious consideration should be given to reducing the dosage or discontinuing therapy when the QTc exceeds 550 msec.

The use of sotalol is contraindicated in patients with hypokalemia (< 4 meq/L). Electrolyte disturbances such as hypokalemia and hypomagnesemia may augment the prolongation effect of sotalol on the QT interval and should be corrected prior to institution of sotalol therapy. In addition, patients who experience frequent, severe, or prolonged diarrhea may be subject to electrolyte losses and should be followed closely and managed accordingly during therapy with sotalol.

Due to their negative inotropic and chronotropic effects on the heart, beta-adrenergic receptor blocking agents (aka beta-blockers) reduce cardiac output and may precipitate or aggravate symptoms of arterial insufficiency in patients with peripheral vascular disease. In addition, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Therapy with beta-blockers should be administered cautiously in patients with peripheral vascular disease. Close monitoring for progression of arterial obstruction is advised.

Sotalol is primarily eliminated by the kidney. Patients with renal impairment may be at greater risk for adverse effects from sotalol, including torsade de pointes and worsened ventricular tachycardia, due to decreased drug clearance. Therapy with sotalol should be administered cautiously in patients with renal impairment. Dosage adjustments (i.e. prolongation of dosing interval) are recommended in patients with moderate to severe renal dysfunction (CrCl <= 60 mL/min), and dosage escalations should occur not more often than after administration of every 5 to 6 doses. Heart rate and ECG, particularly the QTc interval, should be closely monitored.

The use of beta-adrenergic receptor blocking agents (aka beta-blockers) is contraindicated in patients with sinus bradyarrhythmia or heart block greater than the first degree (unless a functioning pacemaker is present). Due to their negative inotropic and chronotropic effects on the heart, the use of beta-blockers is likely to exacerbate these conditions.

Beta-adrenergic blocking agents (beta-blockers), should be used with caution in patients with cerebrovascular insufficiency because of their potential effects relative to blood pressure and pulse. If signs or symptoms suggesting reduced cerebral blood flow are observed, consideration should be given to discontinuing these agents.

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.

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.

Systemic beta-adrenergic receptor blocking agents (aka beta-blockers) may lower intraocular pressure. Therefore, patients with glaucoma or intraocular hypertension may require adjustments in their ophthalmic regimen following a dosing change or discontinuation of beta-blocker therapy.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may alter serum lipid profiles. Increases in serum VLDL and LDL cholesterol and triglycerides, as well as decreases in HDL cholesterol, have been reported with some beta-blockers. Patients with preexisting hyperlipidemia may require closer monitoring during beta-blocker therapy, and adjustments made accordingly in their lipid-lowering regimen.

When beta-adrenergic receptor blocking agents (aka beta-blockers) are used to alleviate symptoms of hyperthyroidism such as tachycardia, anxiety, tremor and heat intolerance, abrupt withdrawal can exacerbate thyrotoxicosis or precipitate a thyroid storm. To minimize this risk, cessation of beta-blocker therapy, when necessary, should occur gradually with incrementally reduced dosages over a period of 1 to 2 weeks. Patients should be advised not to discontinue treatment without first consulting with the physician. Close monitoring is recommended during and after therapy withdrawal.

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.

Beta-adrenergic receptor blocking agents (aka beta-blockers) may potentiate muscle weakness consistent with certain myasthenic symptoms such as diplopia, ptosis, and generalized weakness. Several beta-blockers have been associated rarely with aggravation of muscle weakness in patients with preexisting myasthenia gravis or myasthenic symptoms. Use cautiously in patients with myasthenia gravis.

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.

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.

Administration of beta-blockers alone in the setting of pheochromocytoma has been associated with a paradoxical increase in blood pressure due to the attenuation of beta receptor-mediated vasodilatation in skeletal muscle. In patients with pheochromocytoma, an alpha-blocking agent should be initiated prior to the use of any beta-blocking agent. Caution should be taken in the administration of these agents to patients suspected of having pheochromocytoma.

Agents with non-selective beta-blocking activity may provoke chest pain in patients with Prinzmetal's variant angina. the use of non-selective beta blockers is not recommended in these patients. Caution should be taken in the administration of these agents to patients suspected of having Prinzmetal's variant angina.

The use of beta-blockers in psoriatic patients should be carefully weighed since the use of these agents may cause an aggravation in psoriasis.

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.

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.

Beta-adrenergic blockade in patients with Wolff-Parkinson-White syndrome and tachycardia has been associated with severe bradycardia requiring treatment with a pacemaker. In one case, this result was reported after an initial dose of 5 mg propranolol. The use of beta-adrenergic receptor blocking agents (aka beta-blockers) should be administered cautiously in these patients.