ABSTRACT
Calcium channel blockers (CCBs) are prescribed in a wide variety of cardiovascular conditions. Overdose of this commonly used drug can result in negative physiologic consequences including severe hypotension and even death due to metabolic and hemodynamic compromise. We report the fatal case of an amlodipine overdose, which caused intractable acidosis and cardiovascular failure in a 51-year-old male.
ABSTRACT
BACKGROUND: Acute coronary syndrome (ACS) during postpartum period is rare. In the current manuscript we present a case of a postpartum patient who developed ACS attributed to coronary vasospasm in the absence of vasocontrictive medication or smoking. This condition resolved with intracoronary injection of nitroglycerine and verapamil. CASE: A 26-year-old woman, postpartum day five, presented with a sudden onset of chest pain and an acute ST-segment elevation on ECG. Coronary artery catheterization showed multiple areas of spasm, which was relieved by intracoronary injection of nitroglycerine and verapamil. Post-catheterization hospital stay was uneventful and the patient was discharged in a stable condition. CONCLUSIONS: Early diagnosis and treatment of ACS in the peripartum period is crucial. Vasospastic coronary disease should be included in the differential diagnosis of peripartum chest pain. Nitrates are still considered the best treatment option with or without calcium channel blockers for both recurrence and prevention.
Subject(s)
Acute Coronary Syndrome/diagnostic imaging , Acute Coronary Syndrome/drug therapy , Coronary Vasospasm/drug therapy , Electrocardiography , Nitroglycerin/administration & dosage , Verapamil/administration & dosage , Acute Coronary Syndrome/physiopathology , Adult , Cardiac Catheterization/methods , Chest Pain/diagnosis , Chest Pain/etiology , Coronary Angiography/methods , Coronary Vasospasm/diagnostic imaging , Coronary Vasospasm/physiopathology , Female , Humans , Injections, Intralesional , Obesity, Morbid/diagnosis , Postpartum Period , Pregnancy , Rare Diseases , Risk Assessment , Treatment OutcomeABSTRACT
IMPORTANCE: Heart failure (HF), with or without reduced ejection fraction, and multidrug-resistant hypertension (RHT) are major worldwide health problems of ever-increasing proportions. The mineralocorticoid receptor antagonists (MRAs) spironolactone and eplerenone have proved valuable additions to the overall management of these disorders in patients without significant renal dysfunction. OBSERVATIONS: Neurohormonal activation, including aldosteronism, in HF and RHT, has provided the pathophysiologic basis for the inclusion of MRA in the overall management of these disorders and the respective survival benefit and control of blood pressure. Furthermore, MRAs attenuate the appearance of secondary hyperparathyroidism that accompanies excretory Ca2+ losses induced by aldosteronism in which elevated parathyroid hormone levels raise the risk of adverse cardiovascular events and atraumatic bone fracture. Serial surveillance of serum electrolytes and creatinine levels is mandated to avoid serious hyperkalemia (potassium concentration >5.5 mEq/L) and its attendant risks in patients receiving MRAs. CONCLUSIONS AND RELEVANCE: Mineralocorticoid receptor antagonists are a valuable addition to the practice of medicine. Their judicious use in patients with HF or RHT can improve treatment of these patients.
Subject(s)
Heart Failure/drug therapy , Hypertension/drug therapy , Mineralocorticoid Receptor Antagonists/therapeutic use , Spironolactone/analogs & derivatives , Spironolactone/therapeutic use , Eplerenone , Humans , Hyperkalemia , Ventricular Dysfunction, LeftABSTRACT
Cardiomyocytes must be responsive to demands placed on the heart's contractile work as a muscular pump. In turn, myocyte size is largely dependent on the workload they perform. Both hypertrophied and atrophic myocytes are found in the normal and diseased ventricle. Individual myocytes become atrophic when encumbered by fibrillar collagen, such as occurs at sites of fibrosis. The mechanisms include: (a) being immobilized and subject to disuse with ensuing protein degradation mediated by redox-sensitive, proteolytic ligases of the ubiquitin-proteasome system and (b) dedifferentiated re-expressing fetal genes induced by low intracellular triiodothyronine (T3) via thyroid hormone receptor ß1. This myocyte-selective, low T3 state is a consequence of heterocellular signaling emanating from juxtaposed scar tissue myofibroblasts and their secretome with its de novo generation of angiotensin II. In a paracrine manner, angiotensin II promotes myocyte Ca(2+) entry and subsequent Ca(2+) overload with ensuing oxidative stress that overwhelms antioxidant defenses to activate deiodinase-3 and its enzymatic degradation of T3. In the failing heart, atrophic myocytes represent an endogenous population of viable myocytes which could be rescued to augment contractile mass, reduce systolic wall stress (afterload) and recover ventricular function. Experimental studies have shown the potential for the rescue and recovery of atrophic myocytes in rebuilding the myocardium--a method complementary to today's quest in regenerating myocardium using progenitor cells.
