Effect of Laparoscopic Ovarian Drilling on Anti-Müllerian Hormone Level among Women with Polycystic Ovary Syndrome : A Retrospective Study

Abstract

Background: Thyroid dysfunction is associated with increased cardiovascular morbidity and mortality. Hyperthyroidism increases the susceptibility of the heart to ischemia reperfusion injury. Moreover, myocardial ischemia can be further worsened by increased cardiac workload and oxygen demand elicited by the excess thyroid hormones. Objectives: Investigating the cardiac dysfunction induced by ischemia-reperfusion (IR) in rats exposed to excess thyroid hormones and role of somatostatin analogue against ischemia/reperfusion injury in hyperthyroid rats. Patients and Methods: This study was performed on 24 adult male albino rats of a local strain weighing 140-200 g, allocated into three equal groups: Group I (Control IR group): Euthyroid control group exposed to ischemia-reperfusion. Hearts of this group were isolated and perfused in a Langendorff apparatus. Isolated hearts were subjected to 15 min of stabilization, 20 min of zero-flow global ischemia and 30 min of reperfusion. Group II (Hyperthyroid IR group) were subjected to the same protocol of ischemia reperfusion. Group III (Hyperthyroid IR-OCT group): Hyperthyroid rats were supplemented with the somatostatin analogue, octreotide (OCT), 35 µg/kg subcutaneously, 20 minutes before sacrifice, followed by in-vitro study of cardiac responses to ischemia reperfusion. Blood samples were collected for measurement of plasma free T3, T4 and TSH. Coronary efflux lactate dehydrogenase levels were measured. Also, cardiac tissue malondialdehyde (MDA) levels and tumor necrosis factor alpha (TNF-α) levels were estimated. Results: Hyperthyroid (IR) rats revealed significant elevation in plasma free T3 and T4 with concomitant decrease in TSH levels. A significant reduction in final BW and BW gain were observed with higher absolute weights of left ventricle (LV) and cardiac index compared to the euthyroid controls. Systolic blood pressure (SBP) and mean arterial pressure (MAP) significantly elevated in non-treated hyperthyroid rats with a significant increase in their baseline chronotropic and inotropic activity compared to euthyroid control rats. But after ischemia those rats exhibited significantly higher degree of bradycardia (∆HR) and % change in heart rate (HR) compared to control rats. Moreover, significantly deteriorated post-ischemic recovery of inotropic parameters and significantly higher ∆ changes of these parameters were observed compared to euthyroid controls. These changes were accompanied by significant elevation in coronary efflux LDH levels and both cardiac tissue MDA and TNFα. Meanwhile, octreotide administration to hyperthyroid rats showed improvement of their baseline chronotropic and inotropic parameters as evidenced by the significantly reduced degree of bradycardia as well as significantly lower ∆ change of PT and PT/LV parameters compared to non-treated hyperthyroid rats. Such findings could be ascribed partly to the reduction of oxidative and inflammatory responses to IR as determined by the significantly decreased cardiac tissue MDA and TNFα respectively. Conclusion: Hyperthyroid hearts are less tolerant to ischemia/reperfusion injury with higher susceptibility to oxidative stress as well as overproduction of pro-inflammatory mediators. Thus, pharmacological targets that defend oxidative challenge and confer anti-inflammatory properties, namely octreotide (somatotstatin analogue) are considered to have potential therapeutic effect and may protect against myocardial ischemic damage in hyperthyroidism.