The Effects of Serum Potassium and Magnesium Levels in a Patient with Gitelman's Syndrome on the Timing of Ventricular Wall Motion and the Pattern of Ventricular Strain and Torsion

Abstract

Gitelman's syndrome is a primary renal tubular hypokalemic metabolic alkalosis. Hypokalemia and hypomagnesemia can cause cardiac tissue excitability and conduction. Global ventricular mechanical function is directly related to the contractile properties of cardiac myocytes, which are largely dependent on the flow of ions such as potassium and magnesium. Here, we show that increased levels of potassium, in addition to magnesium, in a patient with Gitelman's syndrome significantly impacts the timing of ventricular wall motion and the pattern of ventricular strain and torsion. Two-dimensional speckle tracking echocardiography was used for evaluation of the hypokalemic-hypomagnesemic period (first day) and third day after potassium chloride and magnesium replacement therapy. The transthoracic echocardiography showed that the percent ejection fraction was similar in hypokalemic-hypomagnesemic (63%) and normokalemic-normomagnesemic (after potassium and magnesium therapy, 67%) hearts. However, decreased left ventricular apical 4-chamber peak systolic longitudinal strain, left ventricle global peak systolic strain, and global torsion values increased after potassium chloride and magnesium replacement therapy.

The Impact of Gitelman Syndrome on Cardiovascular Disease: From Physiopathology to Clinical Management

“…Decreased myocardial contractility with congestive HF due to severe potassium depletion has been reported [ 41 ]. A case report demonstrated that ejection fraction was similar in hypokalemia-hypomagnesemia and normokalaemia-normomagnesemia status (after electrolyte replacement): left ventricular torsion and strain were reduced in the former status but increased after electrolyte replacement [ 42 ].…”