Phosphorus is essential for organic activity such as
Phosphorus is essential for organic activity such as cellular signal transduction, membrane transport, mineral metabolism, and thapsigargin exchange . Bone and teeth store 80% of the total body phosphorus. Intracellular phosphorus consists of the form of organic compounds such as adenosine triphosphate, and free anions like H2PO4− that are referred to as phosphate. Serum phosphorus primarily occurs in the form of inorganic phosphate, which is maintained at a normal range by the regulation of dietary absorption, bone formation, and renal excretion, as well as equilibration with intracellular stores. The most common reason for hyperphosphatemia is inadequate glomerular function in patients with chronic kidney disease . In patients with chronic kidney disease, higher serum phosphate levels are associated with increased risk of cardiovascular diseases . In addition, higher serum phosphate levels, even within normal range, have been associated with a higher risk of cardiovascular disease in patients with prior myocardial infarction . Serum phosphate levels promote vascular injury directly, and are associated with vascular smooth muscle cell calcification, which may increase vascular stiffness and contribute to disease progression. Additionally, higher levels of phosphate are involved in heart failure progression through their interaction with vitamin D, parathyroid hormone, and fibroblast growth factor 23, and also represent a marker of low vitamin D levels . Parathyroid hormone and vitamin D have been linked to heart failure, and are significantly associated with all causes and cardiovascular mortality in CHF patients. In the present study, we could not measure the various factors involved in the metabolism of phosphorus. Larger studies are needed to identify the mechanism by which serum phosphate levels could function as a predictor of responders to CRT, and predicting adverse cardiac events, in patients with CRT-D implantation. The limitations of the present study were that it had a short follow-up period and a small number of patients. Thus, a study with a longer follow-up period and a larger patient population is needed in the future.
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Introduction Takotsubo cardiomyopathy (TC) is a reversible myocardial stunning condition that mimics acute myocardial infarction [1,2]. Patients with TC generally have good prognoses, but some cases are complicated by ventricular arrhythmias associated with prolongation of QT interval . T-wave alternans (TWA) has been reported in patients with pathological conditions who show QT interval prolongation, including long-QT syndrome, myocardial ischemia, and electrolyte disturbances, and is closely associated with the development of ventricular arrhythmias .
Case report The patient was a 74-year-old woman who was transported to the emergency room of our hospital after a transient loss of consciousness. Her electrocardiogram (ECG) showed QT interval prolongation and incessant polymorphic ventricular tachycardia (VT). Blood test results revealed hypokalemia (K+=2.2mEq/L) and cardiac enzyme elevation (troponin I=2.25μg/mL). The patient was administered a slow infusion of magnesium and potassium. Her coronary angiography showed no significant stenosis (Fig. 1A), but ventriculography revealed left ventricular dysfunction with akinesis of the apical wall and compensatory hyperkinesis of the basal wall (Fig. 1B). We diagnosed the patient with TC. In the catheterization room, the frequency of polymorphic VT decreased and her ECG showed significant QT prolongation and beat-to-beat alternans of the J- and T-wave amplitudes with a constant RR interval (Fig. 1C). Prominent J-wave alternans was apparent in leads V2–V6, which lead positions corresponded to the area of akinetic left ventricular segments (Fig. 1C). The beats with higher J-wave amplitude had a shorter QT peak interval than the beats with lower J-wave amplitude with a longer QT peak interval (Fig. 1D). Because of the constant R–R interval with alternating QT intervals, the beats with higher J-wave amplitude had shorter preceding diastolic intervals (DIs) and those with lower J-wave amplitude had longer preceding DIs. The beats with higher J-wave amplitude induced lower systolic blood pressure than those with lower J-wave amplitude (Fig. 2A). A beat with a short coupling interval that showed higher J-point elevation and induced lower ventricular systolic pressure than the preceding beats initiated non-sustained VT (Fig. 2B). This sequence of VT initiation was repeatedly observed. After termination of VT, a beat after a prolonged DI started with a low amplitude J wave and high ventricular pressure followed by alternans of the J wave, TWA, and mechanical alternans (Fig. 2B).