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Verapamil Disease Interactions

There are 12 disease interactions with verapamil.

Major

CCBs (applies to verapamil) aortic stenosis

Major Potential Hazard, High plausibility.

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.

References

  1. "Product Information. Cardene (nicardipine)." Syntex Laboratories Inc (2002):
  2. "Product Information. Adalat (nifedipine)." Bayer (2002):
  3. "Product Information. Procardia (nifedipine)." Pfizer U.S. Pharmaceuticals (2002):
Major

CCBs (applies to verapamil) bradyarrhythmia/AV block

Major Potential Hazard, High plausibility. Applicable conditions: Heart Block, 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.

References

  1. Reams GP, Lau A, Messina C, et al. "Efficacy, electrocardiographic and renal effects of intravenous diltiazem for essential hypertension." Am J Cardiol 60 (1987): i78-84
  2. Nagle RE, Low-Beer T, Horton R "Diltiazem and heart block." Lancet Apr (1989): 907
  3. Imamura T, Koiwaya Y, Nakamura M "Sinoatrial block induced by oral diltiazem." Clin Cardiol 9 (1986): 33-4
  4. Woehler TR, Eff J, Graney W, et al. "Multicenter evaluation of the efficacy and safety of sustained-release diltiazem hydrochloride for the treatment of hypertension." Clin Ther 14 (1992): 148-57
  5. Colombo G, Zucchella G, Planca E, Grieco A "Intravenous diltiazem in the treatment of unstable angina: a study of efficacy and tolerance." Clin Ther 9 (1987): 536-47
  6. Aromatorio GJ, Uretsky BF, Reddy PS "Hypotension and sinus arrest with nifedipine in pulmonary hypertension." Chest 87 (1985): 265-7
  7. Baky SH, Singh BN "Verapamil hydrochloride: pharmacological properties and role in cardiovascular therapeutics." Pharmacotherapy 2 (1982): 328-50
  8. "Product Information. Vascor (bepridil)." McNeil Pharmaceutical (2002):
  9. "Product Information. Cardizem (diltiazem)." Hoechst Marion Roussel (2002):
  10. "Product Information. Calan (verapamil)." Searle (2001):
  11. Andrivet P, Beaslay V, Kiger JP, Gnoc CV "Complete sinus arrest during diltiazem therapy - clinical correlates and efficacy of intravenous calcium." Eur Heart J 15 (1994): 350-4
  12. Gobel EJAM, Hautvast RWM, Vangilst WH, Spanjaard JN, Hillege HL, Dejongste MJL, Molhoek GP, Lie KI "Randomised, double-blind trial of intravenous diltiazem versus glyceryl trinitrate for unstable angina pectoris." Lancet 346 (1995): 1653-7
  13. "Product Information. Covera-HS (verapamil)." Searle (2001):
  14. Pahor M, Manto A, Pedone C, Carosella L, Guralnik JM, Carbonin P "Age and severe adverse drug reactions caused by nifedipine and verapamil." J Clin Epidemiol 49 (1996): 921-8
View all 14 references
Major

CCBs (applies to verapamil) cardiogenic shock/hypotension

Major Potential Hazard, High plausibility.

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.

References

  1. Stehle G, Buss J, Eibach J, et al. "Cardiogenic shock associated with verapamil in a patient with liver cirrhosis." Lancet 336 (1990): 1079
  2. "Product Information. Vascor (bepridil)." McNeil Pharmaceutical (2002):
  3. "Product Information. Cardizem (diltiazem)." Hoechst Marion Roussel (2002):
  4. "Product Information. Calan (verapamil)." Searle (2001):
  5. Kubota K, Pearce GL, Inman WHW "Vasodilation-related adverse events in diltiazem and dihydropyridine calcium antagonists studied by prescription-event monitoring." Eur J Clin Pharmacol 48 (1995): 1-7
  6. Pahor M, Manto A, Pedone C, Carosella L, Guralnik JM, Carbonin P "Age and severe adverse drug reactions caused by nifedipine and verapamil." J Clin Epidemiol 49 (1996): 921-8
View all 6 references
Major

CCBs (applies to verapamil) coronary artery disease

Major Potential Hazard, Low plausibility. Applicable conditions: 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.

References

  1. Schanzenbacher P, Deeg P, Liebau G, Kochsiek K "Paradoxical angina after nifedipine: angiographic documentation." Am J Cardiol 53 (1984): 345-6
  2. Manga P, Vythilingum "Unstable angina precipitated by nifedipine." S Afr Med J 66 (1984): 144
  3. Sia STB, MacDonald PS, Triester B, et al. "Aggravation of myocardial ischaemia by nifedipine." Med J Aust 142 (1985): 48-50
  4. Myrhed M, Wiholm B-E "Nifedipine: a survey of adverse effects." Acta Pharmacol Toxicol (Copenh) 58 (1986): 133-6
  5. Lambert CR, Hill JA, Feldman RL, Pepine CJ "Myocardial ischemia during intravenous nicardipine administration." Am J Cardiol 55 (1985): 844-5
  6. Thomassen AR, Bagger JP, Nielsen TT "Hemodynamic and cardiac metabolic changes during nicardipine-induced myocardial ischemia." Cathet Cardiovasc Diagn 14 (1988): 41-3
  7. "Product Information. Norvasc (amlodipine)." Pfizer U.S. Pharmaceuticals (2002):
  8. "Product Information. Cardene (nicardipine)." Syntex Laboratories Inc (2002):
  9. "Product Information. Procardia (nifedipine)." Pfizer U.S. Pharmaceuticals (2002):
  10. Furberg CD, Psaty BM, Meyer JV "Nifedipine: dose-related increase in mortality in patients with coronary heart disease." Circulation 92 (1995): 1326-31
  11. Kloner RA "Nifedipine in ischemic heart disease." Circulation 92 (1995): 1074-8
  12. Yusuf S "Calcium antagonists in coronary artery disease and hypertension: time for reevaluation?" Circulation 92 (1995): 1079-82
  13. "Product Information. Sular (nisoldipine)." Astra-Zeneca Pharmaceuticals (2001):
  14. Oei SG, Oei SK, Brolmann HAM "Myocardial infarction during nifedipine therapy for preterm labor." N Engl J Med 340 (1999): 154
  15. Abernathy DR, Schwrtz JB "Calcium-antagonist drugs." N Engl J Med 341 (1999): 1447-57
View all 15 references
Major

CCBs (applies to verapamil) liver disease

Major Potential Hazard, High plausibility.

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, several patients have developed cholestasis or hepatocellular injury that was proven by rechallenge. Therapy with CCBs should be administered cautiously and often at reduced dosages in patients with significantly impaired hepatic function. Periodic monitoring of liver function and for excessive pharmacologic effects (e.g., abnormal prolongation of PR interval) is advised, and the dosage adjusted if necessary.

References

  1. Echizen H, Eichelbaum M "Clinical pharmacokinetics of verapamil, nifedipine and diltiazem." Clin Pharmacokinet 11 (1986): 425-49
  2. Saracheck NS, London RL, Matulewicz TJ, et al. "Diltiazem and granulomatous hepatitis." Gastroenterology 88 (1985): 1260-2
  3. Shallcross H, Padley SP, Glynn MJ, Gibbs DD "Fatal renal and hepatic toxicity after treatment with diltiazem." Br Med J 295 (1987): 1256-7
  4. Colombo G, Zucchella G, Planca E, Grieco A "Intravenous diltiazem in the treatment of unstable angina: a study of efficacy and tolerance." Clin Ther 9 (1987): 536-47
  5. Toft E, Vyberg M, Therkelsen K "Diltiazem-induced granulomatous hepatitis." Histopathology 18 (1991): 474-5
  6. Abramson M, Littlejohn GO "Hepatic reactions to nifedipine." Med J Aust 142 (1985): 47-8
  7. Toner M, White A, Moriarty J, Clancy L "Allergic urticarial eruption, leukocytosis and abnormal liver function tests following nifedipine administration." Chest 93 (1988): 1320-1
  8. Babany G, Uzzan F, Larrey D, et al. "Alcoholic-like liver lesions induced by nifedipine." J Hepatol 9 (1989): 252-5
  9. Brodsky SJ, Cutler SS, Weiner DA, Klein MD "Hepatotoxicity due to treatment with verapamil." Ann Intern Med 94 (1981): 490-1
  10. Somogyi A, Albrecht M, Kliems G, et al. "Pharmacokinetics, bioavailability and ECG response of verapamil in patients with liver cirrhosis." Br J Clin Pharmacol 12 (1981): 51-60
  11. Woodcock BG, Rietbrock I, Vohringer HF, Rietbrock N "Verapamil disposition in liver disease and intensive-care patients: kinetics, clearance, and apparent blood flow relationships." Clin Pharmacol Ther 29 (1981): 27-34
  12. Woodcock BG, Rietbrock N "Verapamil bioavailability and dosage in liver disease." Br J Clin Pharmacol 13 (1982): 240-1
  13. Stern EH, Pitchon R, King BD, Wiener I "Possible hepatitis from verapamil." N Engl J Med 306 (1982): 612-3
  14. Stehle G, Buss J, Eibach J, et al. "Cardiogenic shock associated with verapamil in a patient with liver cirrhosis." Lancet 336 (1990): 1079
  15. Hare DL, Horowitz JD "Verapamil hepatotoxicity: a hypersensitivity reaction." Am Heart J 111 (1986): 610-11
  16. Guarascio P, D'Amato C, Sette P, et al. "Liver damage from verapamil." Br Med J 288 (1984): 362-3
  17. Dow RJ, Graham DJM "A reveiw of the human metabolism and pharmacokinetics of nicardipine hydrochloride." Br J Clin Pharmacol 22 (1986): s195-202
  18. McAllister RG Jr, Hamann SR, Blouin RA "Pharmacokinetics of calcium-entry blockers." Am J Cardiol 55 (1985): b30-40
  19. Kates RE "Calcium antagonists: pharmacokinetic properties." Drugs 25 (1983): 113-24
  20. Finucci GF, Padrini R, Piovan D, et al. "Verapamil pharmacokinetics and liver function in patients with cirrhosis." Int J Clin Pharmacol Res 8 (1988): 123-6
  21. Giacomini KM, Massoud N, Wong FM, Giacomini JC "Decreased binding of verapamil to plasma proteins in patients with liver disease." J Cardiovasc Pharmacol 6 (1984): 924-8
  22. Razak TA, McNeil JJ, Sewell RB, Drummer OH, Smallwood RA, Conway EL, Louis WJ "The effect of hepatic cirrhosis on the pharmacokinetics and blood pressure response to nicardipine." Clin Pharmacol Ther 47 (1990): 463-9
  23. Rush WR, Alexander O, Hall DJ, Cairncross L, Dow RJ, Graham DJ "The metabolism of nicardipine hydrochloride in healthy male volunteers." Xenobiotica 16 (1986): 341-9
  24. Benet LZ "Pharmacokinetics and metabolism of bepridil." Am J Cardiol 55 (1985): c8-13
  25. Kurosawa S, Kurosawa N, Owada E, et al. "Pharmacokinetics of diltiazem in patients with liver cirrhosis." Int J Clin Pharmacol Res 10 (1990): 311-8
  26. Elliott HL, Meredith PA "The clinical consequences of the absorption, distribution, metabolism and excretion of amlodipine." Postgrad Med J 67 (1991): s20-3
  27. Stopher DA, Beresford AP, Macrae PV, Humphrey MJ "The metabolism and pharmacokinetics of amlodipine in humans and animals." J Cardiovasc Pharmacol 12 (1988): s55-9
  28. Kleinbloesem CH, van Harten J, Wilson JP, et al. "Nifedipine: kinetics and hemodynamic effects in patients with liver cirrhosis after intravenous and oral administration." Clin Pharmacol Ther 40 (1986): 21-8
  29. Raemsch KD, Sommer J "Pharmacokinetics and metabolism of nifedipine." Hypertension 5 (1983): 18-24
  30. Ramsch KD, Graefe KH, Scherling D, et al. "Pharmacokinetics and metabolism of calcium-blocking agents nifedipine, nitrendipine, and nimodipine." Am J Nephrol 6 (1986): 73-80
  31. Challenor VF, Waller DG, Renwick AG, et al. "The trans-hepatic extraction of nifedipine." Br J Clin Pharmacol 24 (1987): 473-7
  32. Dunselman PH, Edgar B "Felodipine clinical pharmacokinetics." Clin Pharmacokinet 21 (1991): 418-30
  33. Regardh CG, Edgar B, Olsson R, Kendall M, Collste P, Shansky C "Pharmacokinetics of felodipine in patients with liver disease." Eur J Clin Pharmacol 36 (1989): 473-9
  34. Cotting J, Reichen J, Kutz K, Laplanche R, Nuesch E "Pharmacokinetics of isradipine in patients with chronic liver disease." Eur J Clin Pharmacol 38 (1990): 599-603
  35. Tse FL, Jaffe JM "Pharmacokinetics of PN 200-110 (isradipine), a new calcium antagonist, after oral administration in man." Eur J Clin Pharmacol 32 (1987): 361-5
  36. Graham D, Dow R, Hall D, Alexander O, Mroszczak E, Freedman A "The metabolism and pharmacokinetics of nicardipine hydrochloride in man." Br J Clin Pharmacol 20 (1985): s23-8
  37. Gengo FM, Fagan SC, Krol G, Bernhard H "Nimodipine disposition and haemodynamic effects in patients with cirrhosis and age-matched controls." Br J Clin Pharmacol 23 (1987): 47-53
  38. Meredith P, Elliott H "Clinical pharmacokinetics of amlodipine." Clin Pharmacokinet 22 (1992): 22-31
  39. "Product Information. Norvasc (amlodipine)." Pfizer U.S. Pharmaceuticals (2002):
  40. "Product Information. Vascor (bepridil)." McNeil Pharmaceutical (2002):
  41. "Product Information. Cardizem (diltiazem)." Hoechst Marion Roussel (2002):
  42. "Product Information. Plendil (felodipine)." Merck & Company Inc (2002):
  43. "Product Information. Cardene (nicardipine)." Syntex Laboratories Inc (2002):
  44. "Product Information. Procardia (nifedipine)." Pfizer U.S. Pharmaceuticals (2002):
  45. "Product Information. Nimotop (nimodipine)." Bayer (2002):
  46. "Product Information. Calan (verapamil)." Searle (2001):
  47. Johnson KE, Balderston SM, Pieper JA, Mann DE, Reiter MJ "Electrophysiologic effects of verapamil metabolites in the isolated heart." J Cardiovasc Pharmacol 17 (1991): 830-7
  48. "Product Information. Dynacirc (isradipine)." Sandoz Pharmaceuticals Corporation
  49. Kumar KL, Colley CA "Verapamil-induced hepatotoxicity." West J Med 160 (1994): 485-6
  50. Traverse JH, Swenson LJ, Mcbride JW "Acute hepatic injury after treatment with diltiazem." Am Heart J 127 (1994): 1636-9
  51. Scherling D, Karl W, Ahr G, Ahr HJ, Wehinger E "Pharmacokinetics of nisoldipine. III. Biotransformation of nisoldipine in rat, dog, monkey, and man." Arzneimittelforschung 38 (1988): 1105-10
  52. "Product Information. Sular (nisoldipine)." Astra-Zeneca Pharmaceuticals (2001):
  53. Abernathy DR, Schwrtz JB "Calcium-antagonist drugs." N Engl J Med 341 (1999): 1447-57
View all 53 references
Major

Diltiazem/verapamil IV (applies to verapamil) ventricular tachycardia

Major Potential Hazard, High plausibility. Applicable conditions: 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.

References

  1. Buxton AE, Marchlinski FE, Doherty JU, et al. "Hazards of intravenous verapamil for sustained ventricular tachycardia." Am J Cardiol 59 (1987): 1107-10
  2. Winters SL, Schweitzer P, Kupersmith J, Gomes JA "Verapamil-induced polymorphous ventricular tachycardia." J Am Coll Cardiol 6 (1985): 257-9
  3. "Product Information. Calan (verapamil)." Searle (2001):
  4. Braunwald E, Hauser SL, Kasper DL, Fauci AS, Isselbacher KJ, Longo DL, Martin JB, eds., Wilson JD "Harrison's Principles of Internal Medicine." New York, NY: McGraw-Hill Health Professionals Division (1998):
View all 4 references
Major

Verapamil (applies to verapamil) accessory AV tracts

Major Potential Hazard, High plausibility. Applicable conditions: 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.

References

  1. Schwartz JB, Jeang M, Raizner AE, et al. "Accelerated junctional rhythms during oral verapamil therapy." Am Heart J 107 (1984): 440-3
  2. Schwartz JB "Verapamil in atrial fibrillation: the expected, the unexpected, and the unknown." Am Heart J 106 (1983): 173-6
  3. Hame A, Peter T, Platt M, Mandel WJ "Effects of verapamil on supraventricular tachycardia in patients with overt and concealed wolff-parkinson-white syndrome." Am Heart J 101 (1981): 600-12
  4. Jacob AS, Nielsen DH, Gianelly RE "Fatal ventricular fibrillation following verapamil in Wolff-Parkinson-White syndrome with atrial fibrillation." Ann Emerg Med 14 (1985): 159-60
  5. McGovern B, Garan H, Ruskin JN "Precipitation of cardiac arrest by verapamil in patients with Wolff-Parkinson-White syndrome." Ann Intern Med 104 (1986): 791-4
  6. "Product Information. Calan (verapamil)." Searle (2001):
  7. "Product Information. Covera-HS (verapamil)." Searle (2001):
  8. Braunwald E, Hauser SL, Kasper DL, Fauci AS, Isselbacher KJ, Longo DL, Martin JB, eds., Wilson JD "Harrison's Principles of Internal Medicine." New York, NY: McGraw-Hill Health Professionals Division (1998):
View all 8 references
Major

Verapamil (applies to verapamil) CHF/AMI

Major Potential Hazard, High plausibility. Applicable conditions: Congestive Heart Failure, Myocardial Infarction

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.

References

  1. Baky SH, Singh BN "Verapamil hydrochloride: pharmacological properties and role in cardiovascular therapeutics." Pharmacotherapy 2 (1982): 328-50
  2. "Product Information. Calan (verapamil)." Searle (2001):
  3. Pollak A, Falk RH "Left ventricular systolic dysfunction precipitated by verapamil in cardiac amyloidosis." Chest 104 (1993): 618-20
  4. Shimoni A, Maorkendler Y, Neuman Y "Verapamil-induced acute right heart failure." Am Heart J 132 (1996): 193-4
View all 4 references
Major

Verapamil (applies to verapamil) hypertrophic cardiomyopathy

Major Potential Hazard, Moderate plausibility.

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.

References

  1. "Product Information. Calan (verapamil)." Searle (2001):
Moderate

Verapamil (applies to verapamil) neuromuscular transmission

Moderate Potential Hazard, Moderate plausibility. Applicable conditions: Myopathy, 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.

References

  1. "Product Information. Calan (verapamil)." Searle (2001):
  2. "Product Information. Isoptin (verapamil)." Knoll Pharmaceutical Company (2001):
  3. Reverte M "Adverse effect of verapamil in myasthenia gravis: an additional comment." Muscle Nerve 16 (1993): 879-81
Moderate

Verapamil (applies to verapamil) renal dysfunction

Moderate Potential Hazard, High plausibility.

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.

References

  1. Echizen H, Eichelbaum M "Clinical pharmacokinetics of verapamil, nifedipine and diltiazem." Clin Pharmacokinet 11 (1986): 425-49
  2. Mooy J, Schols M, Baak MV, et al. "Pharmacokinetics of verapamil in patients with renal failure." Eur J Clin Pharmacol 28 (1985): 405-10
  3. Pritza DR, Bierman MH, Hammeke MD "Acute toxic effects of sustained-release verapamil in chronic renal failure." Arch Intern Med 151 (1991): 2081-4
  4. Storstein L, Larsen A, Midtbo K, Saevareid L "Pharmacokinetics of calcium blockers in patients with renal insufficiency and in geriatric patients." Acta Med Scand Suppl 681 (1984): 25-30
  5. McAllister RG Jr, Hamann SR, Blouin RA "Pharmacokinetics of calcium-entry blockers." Am J Cardiol 55 (1985): b30-40
  6. Kates RE "Calcium antagonists: pharmacokinetic properties." Drugs 25 (1983): 113-24
  7. "Product Information. Calan (verapamil)." Searle (2001):
  8. Johnson KE, Balderston SM, Pieper JA, Mann DE, Reiter MJ "Electrophysiologic effects of verapamil metabolites in the isolated heart." J Cardiovasc Pharmacol 17 (1991): 830-7
  9. Vazquez C, Huelmos A, Alegria E, Errasti P, Purroy A "Verapamil deleterious effects in chronic renal failure." Nephron 72 (1996): 461-4
View all 9 references
Moderate

Verapamil HS (applies to verapamil) GI narrowing

Moderate Potential Hazard, Moderate plausibility. Applicable conditions: 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.

References

  1. "Product Information. Covera-HS (verapamil)." Searle (2001):

Verapamil drug interactions

There are 591 drug interactions with verapamil.

Verapamil alcohol/food interactions

There are 3 alcohol/food interactions with verapamil.


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Drug Interaction Classification

These classifications are only a guideline. The relevance of a particular drug interaction to a specific individual is difficult to determine. Always consult your healthcare provider before starting or stopping any medication.
Major Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.
Unknown No interaction information available.

Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.