Cardioprotective Effects of Oroxylum indicum Extract Against Doxorubicin and Cyclophosphamide-Induced Cardiotoxicity

SummaryPreinfarction angina and early reperfusion of the infarct-related artery are major determinants of reduced infarct-size in patients with acute myocardial infarction. The beneficial effects of preinfarction angina on infarct size have been attributed to the development of collateral vessels and/or to post-ischemic myocardial protection. However, recently, a relation has been found between prodromal angina, faster coronary recanalization, and smaller infarcts in patients treated with rt-PA: those with preinfarction angina showed earlier reperfusion (p = 0.006) and a 50% reduction of CKMB-estimated infarct-size (p = 0.009) compared to patients without preinfarction angina. This intriguing observation is consistent with a subsequent observation of higher coronary recanalization rates following thrombolysis in patients with prodromal preinfarction angina compared to patients without antecedent angina. Recent findings in dogs show an enhanced spontaneous lysis of plateletrich coronary thrombi with ischemic preconditioning, which is prevented by adenosine blockade, suggesting an antithrom-botic effect of ischemic metabolites. Understanding the mechanisms responsible for earlier and enhanced coronary recanalization in patients with preinfarction angina may open the way to new reperfusion strategies.A vast number of studies, globally involving ≈17,000 patients with acute myocardial infarction, have unequivocally shown that an infarction preceded by angina evolves into a smaller area of necrosis compared to an infarct not preceded by angina (Table 1) (1). So far, preinfarction angina has been thought to have cardioprotective effects mainly through two mechanisms: collateral perfusion of the infarctzone (2-4), and ischemic preconditioning of the myocardium (5-7). Here we discuss a further mechanism of protection represented by improved reperfusion of the infarct-related artery.

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Glutamine Is Cardioprotective in Patients with Ischemic Heart Disease following Cardiopulmonary Bypass

The Heart Surgery Forum ◽

10.1532/hsf98.20111074 ◽

2011 ◽

Vol 14 (6) ◽

pp. 384 ◽

Cited By ~ 17

Author(s):

Vladimir V. Lomivorotov ◽

Sergey M. Efremov ◽

Vladimir A. Shmirev ◽

Dmitry N. Ponomarev ◽

Vladimir N. Lomivorotov ◽

...

Keyword(s):

Heart Disease ◽

Placebo Group ◽

Cardiopulmonary Bypass ◽

Ischemic Heart Disease ◽

Troponin I ◽

Left Ventricular ◽

Ischemic Heart ◽

Left Ventricular Ejection ◽

Study Group ◽

Cardioprotective Effects

Background: The aim of the present study was to investigate the cardioprotective effects of the perioperative use of N(2)-L-alanyl-L-glutamine (GLN) in patients with ischemic heart disease (IHD) who undergo their operations under cardiopulmonary bypass (CPB).Methods: This double-blind, placebo-controlled, randomized study included 50 patients who underwent cardiac surgery with CPB. Exclusion criteria were a left ventricular ejection fraction <50%, diabetes mellitus, <3 months since the onset of myocardial infarction, and emergency surgery. Patients in the study group (n = 25) received 0.4 g/kg GLN (Dipeptiven, 20% solution) per day. Patients in the control group (n = 25) were administered a placebo (0.9% NaCl). The primary end point was the dynamics of troponin I at the following stages: (1) prior to anesthesia, (2) 30 minutes after CPB, (3) 6 hours after CPB, (4) 24 hours after surgery, and (5) 48 hours after surgery. Secondary end points included measurements of hemodynamics with a Swan-Ganz catheter.Results: On the first postoperative day after the surgery, the median troponin I level was significantly lower in the study group than in the placebo group: 1.280 ng/mL (interquartile range [IQR], 0.840-2.230 ng/mL) versus 2.410 ng/mL (IQR, 1.060-6.600 ng/mL) (P = .035). At 4 hours after cardiopulmonary bypass (CPB), the median cardiac index was higher in the patients in the study group: 2.58 L/min per m2 (IQR, 2.34-2.91 L/min per m2) versus 2.03 L/min per m2 (IQR, 1.76-2.32 L/min per m2) (P = .002). The median stroke index also was higher in the patients who received GLN: 32.8 mL/m2 (IQR, 27.8-36.0 mL/m2) versus 26.1 mL/m2 (IQR, 22.6-31.8 mL/m2) (P = .023). The median systemic vascular resistance index was significantly lower in the study group than in the placebo group: 1942 dyn�s/cm5 per m2 (IQR, 1828-2209 dyn�s/cm5 per m2) versus 2456 dyn�s/cm5 per m2 (IQR, 2400-3265 dyn�s/cm5 per m2) (P = .001).Conclusion: Perioperative administration of GLN during the first 24 hours has cardioprotective effects in IHD patients following CPB. This technique enhances the troponin concentration at 24 hours after surgery and is associated with improved myocardial function.

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1031-P: Impact of the Cardioprotective Effects of GLP-1 Agonists in the Management of Diabetes

Diabetes ◽

10.2337/db19-1031-p ◽

2019 ◽

Vol 68 (Supplement 1) ◽

pp. 1031-P

Author(s):

SHAYAN S. MAHAPATRA ◽

CRISTIAN MILLA-MATUTE ◽

CARMEN V. VILLABONA ◽

LUIS CARABALLO

Keyword(s):

Cardioprotective Effects

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CARDIOPROTECTIVE EFFECTS TO CHRONIC ADMINISTRATION OF GOMPHRENA GLOBOSA FLOWERS IN ISOPROTERENOL INDUCED MYOCARDIAL INFARCTION: BIOCHEMICAL, HISTOPATHOLOGICAL AND ULTRASTRUCTURAL STUDIES

International Journal of Pharmaceutical Research ◽

10.31838/ijpr/2019.11.02.071 ◽

2019 ◽

Vol 11 (02) ◽

Keyword(s):

Myocardial Infarction ◽

Chronic Administration ◽

Ultrastructural Studies ◽

Gomphrena Globosa ◽

Cardioprotective Effects

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Mechanisms underlying heart failure in type 2 diabetes mellitus

Heart and Metabolism - Heart Failure in patients with Diabetes ◽

10.31887/hm.2019.80/hbugger ◽

2019 ◽

pp. 37-39

Keyword(s):

Diabetes Mellitus ◽

Heart Failure ◽

Experimental Studies ◽

Vascular Complications ◽

Molecular Alterations ◽

Increased Risk ◽

Cardioprotective Effects ◽

Underlying Mechanisms ◽

Cardio Vascular

The prevalence of heart failure is markedly increased in individuals with diabetes mellitus. Numerous observational studies suggest that this increased risk for heart failure can be attributed to exacerbated vascular complications and the presence of increased risk factors in diabetic subjects. In addition, experimental studies revealed the presence of a number of distinct molecular alterations in the myocardium that occur independently of vascular disease and hypertension. Many of these molecular alterations are similarly observed in failing hearts of nondiabetic patients and have thus been proposed to contribute to the increased risk for heart failure in diabetes. The interest in understanding the underlying mechanisms of impaired cardio- vascular outcomes in diabetic individuals has much increased since the demonstration of cardioprotective effects of SGLT-2 inhibitors and GLP-1 receptor agonists in recent clinical trials. The current review therefore summarizes the distinct mechanisms that have been proposed to increase the risk for heart failure in diabetes mellitus.

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