This patient demonstrated a severe, acute reversible abnormality of myocardial function, the cause of which is not clear. Marked improvement occurred, temporally related to the removal of her necrotic remnant kidney. Sepsis has been demonstrated to be associated with decreased LV ejection fraction and elevated LV end-diastolic volume despite increased cardiac output. These findings may be due to deranged coronary blood flow with reduced oxygen extraction or to the effects of circulating myocardial depressant substances. At present, there is no consensus regarding the identity or relative importance of these factors, which may include a 20-kd water-soluble molecule, and cytokines such as interleukin 25 and TNF. A cytokine response similar to that in sepsis occurs in nonseptic inflammation and it is conceivable that myocardial suppression may occur in this context. This patient demonstrated the clinical features of the systemic inflammatory response syndrome, namely temperature > 38.0°C, white blood cell count > 12,000/cu mm, and heart rate > 90/min, in the absence of evidence of sepsis. Presumably the necrotic kidney was responsible for such an inflammatory reaction. canadian family pharmacy online
The entity of a reversible uremic cardiomyopathy was first suggested in 1967, but cardiac failure in these patients may also be attributable to a number of other factors such as fluid overload and hypertension. However, a study of patients with renal failure and congestive heart failure demonstrated that a subgroup had echocardiographic LV dysfunction that improved after hemodialysis, suggesting the role of a uremic toxin. Reversal of LV dysfunction has also been demonstrated following renal transplantation.” These mechanisms are unlikely to have been responsible for this patient’s LV dysfunction as she had undergone dialysis twice prior to the onset of clinical cardiac failure and the improvement was not temporally related to dialysis. Hyperparathyroidism in renal failure may cause LV dysfunction reversed by parathyroidectomy. As this effect of hyperparathyroidism has been demonstrated only in patients with renal failure, it may be a combined effect of the two disorders.
A review of the literature reveals a number of other causes of nonischemic reversible myocardial suppression (Table 2). Although the finding of severe systolic ventricular dysfunction is often attributed to irreversible myocardial damage, the possibility of a reversible condition should be considered, as many require specific interventions. Acute viral myocarditis may cause this clinical entity with a wide variability in outcome, from complete reversal to progressive deterioration resulting in chronic dilated cardiomyopathy. Catecholamine excess, either endogenously secreted as in pheochromocytoma or administered therapeutically may cause clinically significant reversible contractile depression. Various drugs and toxins may act via similar mechanisms to induce transient contractile abnormalities (Table 2). Electrolyte disorders can reversibly depress myocardial function. These include hypocalcemia, calcium being required for excitation-contraction coupling, and hypophosphatemia, presumably by depletion of intracellular adenosine triphosphate. Reversible cardiomyopathy may also occur as part of acute pernicious beriberi, caused by thiamine deficiency. Other conditions, including thyroid disease, selenium deficiency, hemochromatosis, and alcohol and drug toxicity may cause myocardial contractile dysfunction on a more long-term time-scale, but with significant reversibility (Table 2).
Table 2—Carnes of Reversible Myocardial Contractile Depression
|1.||Sepsis and systemic inflammatory response syndrome|
|2.||Drugs and toxins:EpinephrineAmphetamine, cocaine, fenfluramineScorpion venom
Hyperparathyroidism (with renal failure) Hypoparathyroidism
|4.||InflammatoryAcute myocarditis Cardiac transplant rejection|
|6.||Nutritional Thiamine deficiency Selenium deficiency|
|7.||MiscellaneousHemochromatosis Renal failure9 lo Pos ttachycardia Anaphylaxis|