cardiovascular-agents and Rhabdomyolysis

Critical limb ischemia refers to the clinical state of advanced arterial occlusive disease, placing an extremity at risk for gangrene and limb loss. Critical limb ischemia has 2 broad clinical subcategories that are vital to differentiate: acute limb ischemia and chronic arterial occlusive disease. This article reviews the etiologies, diagnosis, and treatment of critical limb ischemia.

Topics: Acute Disease; Arterial Occlusive Diseases; Cardiovascular Agents; Chronic Disease; Compartment Syndromes; Endarterectomy; Equipment Design; Humans; Ischemia; Lower Extremity; Magnetic Resonance Angiography; Reperfusion; Rhabdomyolysis; Thrombectomy; Thrombolytic Therapy; Tomography, X-Ray Computed; Upper Extremity

Rhabdomyolysis precipitated by multitherapy is most frequently described during statin treatment, due to impairment of statin clearance by drugs sharing cytochrome P450 biotransformation pathway. Modulation of membrane transporters for drug efflux, operated by substrates, can also affect drugs' tissue levels. We report rhabdomyolysis in an elderly patient, in multitreatment with different potentially myotoxic medications, taking place seven months after atorvastatin discontinuation. Affected by ischaemic heart disease, arterial hypertension and dementia-related behaviour disturbances, the patient was receiving angiotensin 2-receptor inhibitors, beta-blockers, vasodilators, diuretics, salycilates, allopurinol, proton pump inhibitors, antipsychotics and antidepressants. He had taken atorvastatin for 14 years, with constantly normal creatine-kinase plasma levels. Two months after addition of the antianginal drug ranolazine, creatine-kinase mildly increased and atorvastatin was withdrawn. Nonetheless, creatine-kinase progressively rose, with severe weakness and rhabdomyolysis developing seven months later. Muscle biopsy showed a necrotizing myopathy with no inflammation or autoimmune changes. After ranolazine withdrawal, creatine-kinase and myoglobin returned to normal levels and strength was restored. Several psychotropic and cardiovascular medications prescribed to the patient share either cytochrome P450 biotransformation and permeability-glycoprotein efflux transport. In the event of cardiovascular/neuropsychiatric polypharmacy in geriatric patients, the risk of muscle severe adverse effects from pharmacokinetic drug-drug interaction should be considered beyond the direct myotoxicity of statins.

Topics: Aged; Cardiovascular Agents; Drug Interactions; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Psychotropic Drugs; Rhabdomyolysis; Substance Withdrawal Syndrome

To report a case of rhabdomyolysis and acute hepatitis associated with the coadministration of atorvastatin and diltiazem.. A 60-year-old African American man with a significant past medical history presented to the emergency department with acute renal failure secondary to rhabdomyolysis. In addition, liver enzymes were elevated to greater than 3 times normal. The only change in medication was the initiation of diltiazem 3 weeks earlier for atrial fibrillation to a complicated medication regimen that included atorvastatin.. Rhabdomyolysis has been reported in patients receiving hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors when coadministered with agents that may inhibit their metabolism. Atorvastatin is the most potent of this class of agents currently available and is commonly used in the treatment of hyperlipidemia. Rhabdomyolysis resulting from the drug interaction between diltiazem and other HMG-CoA reductase inhibitors has been described in the literature. However, no report has specifically associated this adverse event with atorvastatin and diltiazem. We describe a patient with a complex medication regimen who was admitted for rhabdomyolysis and accompanying acute renal failure, along with acute hepatitis, thought to be secondary to a drug interaction between atorvastatin and diltiazem.. While optimizing the patient's lipid profile should be the primary factor in choosing one statin over another, the potential for drug interactions requires close attention. All patients beginning HMG-CoA reductase inhibitor therapy should be counseled regarding the signs and symptoms of muscle injury; particular attention should be paid to those patients who are taking medications that may interact.

Topics: Acute Disease; Acute Kidney Injury; Atorvastatin; Cardiovascular Agents; Chemical and Drug Induced Liver Injury; Diltiazem; Drug Interactions; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Male; Middle Aged; Pyrroles; Rhabdomyolysis