Cardiac remodeling of viable myocardium occurs after acute myocardial infarction (AMI) and further contributes to cardiac dysfunction. The present study explored whether thyroid hormone (TH) administered shortly after AMI in rats can attenuate cardiac remodeling and improve cardiac function. TH regulates important structural and regulatory proteins in the myocardium including myosin isoform expression and calcium cycling proteins. AMI was induced in Wistar male rats by ligating left coronary artery (AMI, n=10), while sham-operated rats were used as controls (SHAM, n=10). Animals with acute myocardial infarction were also treated with 0.05% thyroid powder in food (AMI-THYR, n=10). Within 2 weeks, cardiac function was impaired as assessed by echocardiography and under isometric conditions in Langendorff preparations. Ejection fraction (EF%) was 71.5 (SEM, 2.7) in SHAM versus 30.0 (2.0) in AMI, P<0.05. +dp/dt was 3886 (566) in SHAM versus 2266 (206) in AMI hearts, P<0.05 and -dp/dt was 1860 (46) in SHAM versus 1633 (120) in AMI hearts, P=ns. Such changes were associated with alterations in myosin isoform expression in the non-infarcted area; AMI hearts expressed 34% alpha-MHC and 66% beta-MHC versus 52% alpha-MHC and 48% beta-MHC in SHAM, P<0.05, while the expression of SERCA and phospholamban (PLB) remained unchanged. Furthermore, a mismatch of left ventricular size and cardiac mass (2*Posterior Wall thickness/LVIDd was decreased) was observed. After TH treatment, AMI-THYR hearts expressed 71% alpha-MHC and 29% beta-MHC, P<0.05 versus SHAM and AMI and the ratio of SERCA/PLB was increased by 2.0-fold, P<0.05 versus SHAM and AMI. These changes corresponded to a marked improvement in cardiac function; EF% was raised to 45.8 (1.7), P<0.05 versus AMI while +dp/dt and -dp/dt were 3800 (435) and 2600 (200), respectively, in AMI-THYR hearts, P<0.05 versus AMI. The ratio of 2*Posterior Wall thickness/LVIDd was normalized. Thyroid hormone administration early after infarction attenuates cardiac remodeling and significantly improves myocardial performance.

We have previously shown that long-term thyroxine administration can protect the heart against ischemia. In the present study, we investigated whether thyroxine-induced cardioprotection can mimic the pattern of protection that is afforded by a well-established cardioprotective means such as ischemic preconditioning. In a Langendorff-perfused rat heart preparation, after an initial stabilization, normal and thyroxine-treated hearts were subjected to 20 minutes of zero-flow global ischemia followed by 45 minutes of reperfusion. In thyroxine-treated hearts, phospho-p38 mitogen-activated protein kinase (MAPK) was found to be less at the end of the ischemic period, whereas ischemic contracture was accelerated and postischemic recovery was increased in comparison to normal hearts. In addition, normal hearts were subjected to a four-cycle preconditioning protocol before ischemia. Phospho-p38 MAPK was found to be less at the end of the ischemic period in preconditioned hearts, whereas ischemic contracture was accelerated and postischemic functional recovery was increased in those hearts in comparison to nonpreconditioned hearts. An increase in basal expression and phosphorylation of PKCδ was also found to occur after long-term thyroxine administration. We conclude that long-term thyroxine administration can protect the heart from ischemic injury through a pattern of protection that closely resembles that of ischemic preconditioning.

Objective: This study investigated whether changes in thyroid hormone (TH) in plasma are associated with the recovery of cardiac function in patients with acute myocardial infarction (AMI). Previous experimental studies have provided evidence of potential implication of TH signaling in post-ischemic recovery of cardiac function.Methods: A total of 47 patients with AMI and early reperfusion therapy were included in this study. Myocardial injury was analyzed by peak creatinine kinase–MB (CKMB) and cardiac function was assessed by echocardiographic left ventricular ejection fraction (LVEF%). Recovery of function (ΔEF%) was estimated as the difference of LVEF% between 48 h and 6 months (6 mo) after AMI. Total triiodothyronine (T₃), thyroxine (T₄), and TSH were measured in plasma at different time points (24 h, 48 h, 5 d, and 6 mo).Results: A significant correlation between LVEF% and T₃ (r=0.5, P=0.0004) was found early after AMI (48 h), whereas no correlation was observed between CKMB and T₃ (r=−0.04, P=0.81). A strong correlation was found between ΔEF% and total T₃ (r=0.64, P=10⁻⁶) at 6 mo after AMI. Furthermore, multivariate regression analysis revealed that T₃ at 6 mo (r=0.64, r²=0.41, P=10⁻⁶) was an independent determinant of ΔEF%.Conclusion: Changes in T₃ levels in plasma are closely correlated with the early and late recovery of cardiac function after AMI. T₃ levels at 6 mo appear to be an independent predictor of late functional recovery.

Hypertensive crises (76% urgencies, 24% emergencies) represented more than one fourth of all medical urgencies/emergencies. Hypertensive urgencies frequently present with headache (22%), epistaxis (17%), faintness, and psychomotor agitation (10%) and hypertensive emergencies frequently present with chest pain (27%), dyspnea (22%) and neurological deficit (21%). Types of end-organ damage associated with hypertensive emergencies include cerebral infarction (24%), acute pulmonary edema (23%) and hypertensive encephalopathy (16%), as well as cerebral hemorrhage (4.5%). The most important factor that limits morbidity and mortality from these disorders is prompt and carefully considered therapy. Unfortunately, hypertensive emergencies and urgencies are among the most misunderstood and mismanaged of acute medical problems seen today. The primary goal of intervention in a hypertensive crisis is to safely reduce BP. Immediate reduction in BP is required only in patients with acute end-organ damage (i.e. hypertensive emergency). This requires treatment with a titratable short-acting intravenous (IV) antihypertensive agent, while severe hypertension with no acute end-organ damage is usually treated with oral antihypertensive agents. Patients with hypertensive emergencies are best treated in an intensive care unit (ICU) with titratable IV hypotensive agents. The aim of this review is to summarize the details regarding the definition-impact, causes, clinical condition and management of hypertensive crises.