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 Mustafa Yildiz, M.D., Ph.D.,* Banu Sahin Yildiz, M.D.,† Suleyman Karakoyun, M.D.,* Sinem Cakal, M.D.,* Alparslan Sahin, M.D.,‡ and Nazire Baskurt Aladag, M.D.† *Department of Cardiology, Kartal Kosuyolu Yüksek Ihtisas Educational and Research Hospital,İIstanbul, Turkey; †Department of Internal Medicine, Dr Lutfi Kırdar Kartal Educational and Research Hospital,İIstanbul, Turkey; and ‡Department of Cardiology, Bakirkoy Dr. Sadi Konuk Education and Research Hospital,İIstanbul, Turkey 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 depen- dent 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. (Echocardiography 2013;30:E47-E50) Key words: Gitelman’s syndrome, potassium, magnesium, ventricular strain and torsion Gitelman’s syndrome is linked to inactivating mutations in the SLC12A3 gene resulting in a loss of function of the encoded thiazide-sensi- tive sodium chloride co-transporter. 1 Biochemi- cally, there is metabolic alkalosis, profound hypokalemia, hypomagnesaemia, and hypocal- ciuria. Replacement therapy is the main treat- ment for Gitelman’s syndrome, which means magnesium supplementation throughout life. Also correction of hypokalemia may occasionally require the addition of potassium salts and/or anti-aldosterone drugs such as spironolactone or amiloride. 1 Hypokalemia and hypomagnese- mia can cause myocardial contractility that might be associated with an increased influx of calcium (Ca ++ ) as a result of hypokalemia- induced inhibition of sarcolemmal magnesium (Mg ++ )-dependent, Na + -K + -ATPase. 2 Myocardial torsion dynamics, myocardial strain, and syn- chronicity of myocardial contraction can be determined with Doppler tissue imaging echo- cardiography. 3 Global ventricular mechanical function is directly related to the contractile properties of cardiac myocytes, which are lar- gely 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. Case Report: A 28-year-old woman was admitted to our clinic with weakness and cramps of all 4 limbs. Cardiovascular examination was normal with sinus rhythm and no murmur. There was no Address for correspondence and reprint requests: Mustafa Yıldız, M.D., Ph.D., Department of Cardiology, Kartal Kosuyo- lu Yüksek Ihtisas Educational and Research Hospital, 34846 Kartal, Istanbul, Turkey. Fax: +90-(212)-459-20-69; E-mail: mustafayilldiz@yahoo.com E47 © 2012, Wiley Periodicals, Inc. DOI: 10.1111/echo.12034 Echocardiography