Michael S. Zawaneh

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Scholarly Contributions

Chapters

• Zawaneh, M. (2011). Risk Stratification for Stroke in Patients with Atrial Fibrillation. In Cardiovascular Consults, Vol. 1 No. 2.

Journals/Publications

• Faulx, M. D., Chandler, M. P., Zawaneh, M. S., Stanley, W. C., & Hoit, B. D. (2021). Mouse strain-specific differences in cardiac metabolic enzyme activities observed in a model of isoproterenol-induced cardiac hypertrophy. Clinical and experimental pharmacology & physiology, 34(1-2), 77-80.
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  1. Alterations in myocardial energy metabolism accompany pressure overload-induced hypertrophy. We previously described a novel model of catecholamine-induced hypertrophy in which A/J mice exhibit more robust cardiac hypertrophy than B6 mice. Accordingly, we assessed the influence of mouse strain on the activities of key myocardial metabolic enzymes and whether there are strain-related metabolic adaptations to short-term, high-dose isoproterenol (ISO) administration. 2. Thirty-nine male mice (19 A/J mice, 20 B6 mice), aged 12-15 weeks, were randomly assigned to receive either ISO (100 mg/kg, s.c.) or vehicle (sterile water) daily for 5 days. On Day 6, all hearts were excised, weighed, freeze clamped and assayed for pyruvate dehydrogenase (PDH), medium chain acyl-CoA dehydrogenase, carnitine palmitoyl transferase I and citrate synthase activities. Plasma fatty acids (FA) were also measured. 3. The ISO-treated A/J mice demonstrated greater percentage increases in gravimetric heart weight/bodyweight ratio than ISO-treated B6 mice (24 vs 3%, respectively; P < 0.001). All enzyme activities were significantly greater in vehicle-treated B6 mice than in A/J mice, illustrating a greater capacity for aerobic metabolism in B6 mice. Administration of ISO reduced PDHa (active form) activity in B6 mice by 47% (P < 0.001), with no significant change seen in A/J mice. Free FA levels were not significantly different between groups; thus, the differences in PDHa were not due to changes in FA. 4. The basal activity of myocardial metabolic enzymes is greater in B6 mice than in A/J mice and ISO alters myocardial PDH activity in a mouse strain-dependent manner. Compared with A/J mice, B6 mice demonstrate less ISO-induced cardiac hypertrophy, but greater activity of key enzymes regulating FA and carbohydrate oxidation, which may protect against the development of hypertrophy. The metabolic adaptations associated with ISO-induced hypertrophy differ from those reported with pressure overload hypertrophy.
• Tomaiko, E., & Zawaneh, M. S. (2021). Cybersecurity threats to cardiac implantable devices: room for improvement. Current opinion in cardiology, 36(1), 1-4.
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  For over a decade, vulnerabilities in the healthcare industry have been identified. Medical devices such as cardiovascular implantable electronic devices (CIEDs) are particularly concerning because of direct threats to patient safety and protected health information (PHI). Although these vulnerabilities have been identified and changes have been made, there is significant room for improvement. We identify changes and improvements to be made in the industry, by providers, and by patients.
• Zawaneh, M. S., & Stambler, B. S. (2010). Chronic Suppression of Ventricular Tachyarrhythmias in Patients with ICDs. Cardiac electrophysiology clinics, 2(3), 443-457.
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  In this review, we examine the data evaluating the role of adjuvant therapy with antiarrthymic drugs (AADs) in chronic suppression of ventricular tachyarrhythmias in the patient with an ICD. It must be noted that all uses of AADs for this indication represent "off-label" prescription. No AAD is approved by the Food and Drug Administration (FDA) specifically as a therapy to reduce ICD shocks.
• Morgan, E. E., Faulx, M. D., McElfresh, T. A., Kung, T. A., Zawaneh, M. S., Stanley, W. C., Chandler, M. P., & Hoit, B. D. (2004). Validation of echocardiographic methods for assessing left ventricular dysfunction in rats with myocardial infarction. American journal of physiology. Heart and circulatory physiology, 287(5), H2049-53.
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  The rat infarct model is widely used in heart failure research, but few echocardiographic indexes of left ventricular (LV) function are validated in this model. Accordingly, the objective of this study was to validate a 13-segment LV wall motion score index (WMSI) and the myocardial performance index (MPI) in infarcted rats. Twenty-nine male Wistar rats underwent left coronary artery ligation or sham operation and were evaluated with two-dimensional and Doppler flow echocardiography 8 wk later. After echocardiography, invasive indexes were obtained using a high-fidelity catheter. WMSI and MPI were correlated with the invasive and noninvasive measurements of LV function. WMSI and MPI significantly correlated directly with end-diastolic pressure (r=0.72 and 0.42 for WMSI and MPI, respectively) and the time constant of isovolumic relaxation (r=0.68 and 0.48) and inversely with peak rate of rise of LV pressure (+dP/dt; r=-0.68 and -0.50), peak rate of decline in LV pressure (r=-0.57 and -0.44), LV developed pressure (r=-0.58 and -0.42), area fractional shortening (r=-0.85 and -0.53), and cardiac index (r=-0.74 and -0.74). Stepwise linear regression analyses revealed that LV end-diastolic pressure, +dP/dt, area fractional shortening, and cardiac index were independent determinants of WMSI (r=0.994) and that cardiac index and +dP/dt were independent determinants of MPI (r=0.781). We conclude that the 13-segment WMSI and MPI are reproducible and correlate strongly with established echocardiographic and invasive indexes of systolic and diastolic function. These findings support the use of WMSI and MPI as indexes of global LV function in the rat infarction model of heart failure.