From vulnerable plaque to blood healthy therapy.

Cardiovascular atherosclerotic disease is the leading cause of death in China and in Western nations. People with plaque or stenosis in the coronary artery or the carotid artery are the most susceptible population to suffer from acute events. Current investigations showed that plaque with the characteristics of intra-plaque hemorrhage or a thin cap with a large lipid core was causally associated with vulnerable plaque and plaque rupture.

Absence of myocyte regeneration by mobilization of bone marrow stem cells after myocardial infarction.

The study aimed to test the potential for bone marrow stem cells (BMSC) mobilized by granulocyte macrophage colony stimulating factor (GM-CSF) to promote neovascularization and cardiomyocytes regeneration in a rat model of myocardial infarction. The myocardial infracted rats were randomly assigned to receive GM-CSF injection as GM-CSF group or received saline injection as control group. Evaluation of CD34 stem cells was performed by flow cytometry.

Chronic pretreatment of metformin is associated with the reduction of the no-reflow phenomenon in patients with diabetes mellitus after primary angioplasty for acute myocardial infarction.

Introduction: Metformin is one of the most commonly prescribed antihyperglycemic agents for the treatment of type 2 diabetes. However, little is known about the effect of metformin on no-reflow in diabetic patients.

Aim: In this study, we investigated retrospectively whether chronic pretreatment with metformin was associated with no-reflow in diabetic patients who underwent primary coronary intervention for acute myocardial infarction (AMI).

Alteration of parasympathetic/sympathetic ratio in the infarcted myocardium after Schwann cell transplantation modified electrophysiological function of heart: a novel antiarrhythmic therapy.

Background: Neural remodeling after myocardial infarction (MI) may cause fatal ventricular arrhythmia. Schwann cells (SCs), which are important for neurogenesis, are dramatically reduced after MI. We investigated the feasibility of modifying nervous system regeneration after MI and the efficacy by which it may prevent ventricular arrhythmia following SC transplantation.

Diagnosis, operation, recurrence, metastasis, and death: a case of primary cardiac rhabdomyosarcoma.

We present a case report of a 48-year-old man with a huge left atrial rhabdomyosarcoma who presented as severe mitral stenosis and accepted emergency surgery. Two years later, a pathologic fracture revealed osseous metastasis, and intracardiac recurrence was detected by echocardiography. The patient died of multiple organ failure in the end.

The effect of statins on the no-reflow phenomenon: an observational study in patients with hyperglycemia before primary angioplasty.

Background: An association between admission plasma glucose levels and an increased risk of no-reflow has been well documented. Although HMG-CoA reductase inhibitor (statin) therapy can reduce no-reflow, little is known about its effect on no-reflow in patients with hyperglycemia. In the present study, we investigated whether pretreatment with a statin could reduce no-reflow in patients with hyperglycemia, who underwent primary coronary intervention for acute myocardial infarction (AMI).

Carvedilol reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+ channel.

It has been verified that carvedilol can attenuate myocardial no-reflow. However, the effects of carvedilol on adenosine triphosphate-sensitive K(+) (K(ATP)) channel and endothelin-1 (ET-1) are unknown. Forty mini-swines were randomized into 5 study groups: 8 control, 8 carvedilol pretreatment, 8 glibenclamide (K(ATP) channel blocker)-treated, 8 carvedilol and glibenclamide-pre-treated and 8 sham-operated.

Intravenous adenosine reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+ channel.

Unlabelled: It has been verified that adenosine can attenuate myocardial no-reflow. However, the effects of adenosine on adenosine triphosphate-sensitive K+ (KATP) channel and endothelin-1 (ET-1) are unknown.

Methods: Forty mini-swines were randomized into 5 study groups: 8 in the control group, 8 in the adenosine pretreatment group, 8 in the glibenclamide (K(ATP) channel blocker)-treated group, 8 in the adenosine and glibenclamide-pretreated group and 8 in the sham-operated group.

Remote periconditioning reduces myocardial no-reflow by the activation of K ATP channel via inhibition of Rho-kinase.

Unlabelled: Remote periconditioning is induced by brief cycles of ischemia and reperfusion of a remote organ applied during sustained myocardial ischemia. It remains unknown whether the remote periconditioning reduces myocardial no-reflow. The adenosine triphosphate-sensitive potassium (K(ATP)) channel opening and inhibition of Rho-kinase may be the important mechanism of protection against myocardial no-reflow.

Effect of statin therapy on reperfusion arrhythmia in patients who underwent successful primary angioplasty.

Background: In animal models, pretreatment with statin can prevent reperfusion arrhythmia. In the observational study, we investigated whether pretreatment with statin may prevent reperfusion arrhythmia in patients who underwent primary coronary intervention for acute myocardial infarction (AMI).

Method And Results: A total of 226 consecutive patients who underwent successful primary angioplasty for a first AMI were studied.

Intravenous nicorandil preserves endothelial junctions by decreasing endothelin-1 via activation of ATP-sensitive K+ channel.

Background: It has been verified that nicorandil can attenuate myocardial no-reflow. However; the effects of nicorandil on endothelial junctions and Endothelin-1 (ET-1) are unknown.

Methods: 40 mini-swines randomized into 5 study groups: 8 in control, 8 nicorandil pretreatment, 8 in glibenclamide (KATP channel blocker)-treated, 8 in nicorandil and glibenclamide-pretreated and 8 in sham-operated.

Is elevated high-density lipoprotein cholesterol always good for coronary heart disease?

Background: High-density lipoprotein (HDL) could enhance inflammation in atherogenesis when inflammatory response is present, and the activity of paraoxonase and antioxidant in HDL in the elderly is significantly decreased. There might be a different role for high-density lipoprotein cholesterol (HDL-C) between different age groups in patients with coronary heart disease (CHD).

Methods: For this study, 225 inpatients with CHD (coronary atherosclerosis stenosis >/= 50% on >/= 1 major coronary arteries by coronary angiography), and 80 without CHD; 120 resting unstable angina patients, and 68 with stable angina were consecutively recruited.

Development of the functionally total artificial heart using an artery pump.

Based on the assumption that only the pump function of the diseased heart should be assisted or replaced by device while resecting the native heart is unnecessary, the concept of a "functionally total artificial heart (FTAH)" was explored. An artery pump (AP) was designed for the FTAH. The fabricated pattern of the AP, having an outer diameter of 28 mm and a length of 42 mm, was implanted in the position of ascending aorta or pulmonary trunk, joining in series to the chambers of the left ventricle or the right ventricle.

Chronic pretreatment of ACEI reduces no-reflow in patients with acute myocardial infarction treated with primary angioplasty.

Background: In animal models, pretreatment with angiotensin-converting enzyme inhibitor (ACEI) can reduce no-reflow. In the present study, we investigated whether pretreatment with ACEI may prevent no-reflow in patients who underwent primary coronary intervention for AMI.

Method And Results: A total of 259 consecutive patients who underwent primary angioplasty for a first AMI were studied.

Apolipoprotein E polymorphism influences lipid phenotypes in Chinese families with familial combined hyperlipidemia.

Background: Apolipoprotein E (apoE) polymorphism is associated with changes in the lipoprotein profile of individuals with familial combined hyperlipidemia (FCHL), but its effects on the lipoprotein profiles of members of Chinese families with FCHL remain uncertain.

Methods And Results: 43 FCHL families (n=449) and 9 normolipidemic families (n=73) were recruited to assess the influence of apoE polymorphism on plasma lipids. The relative frequency of the epsilon4 allele in affected and unaffected FCHL relatives, spouses and normolipidemic members was 13.

Patients with low high-density lipoprotein-cholesterol or smoking are more likely to develop myocardial infarction among subjects with a visible lesion or stenosis in coronary artery.

Background: Traditional contrast coronary arteriography affords only an indirect view of aspects of atheromata related to their propensity to trigger thromboses, so it is urgent to recognize the vulnerable person who is more likely to develop myocardial infarction (MI) among patients with visible lesion or stenosis in coronary artery.

Methods And Results: Two hundred and eighty-eight patients (144 MI patients, 144 controls) who had either a visible lesion or differing extent of stenosis in 1 or more major coronary arteries were consecutively enrolled. Lipid profile, C-reactive protein (CRP), smoking, hypertension, dyslipidemia and diabetes were analyzed for their association with MI.

Different effects of postconditioning on myocardial no-reflow in the normal and hypercholesterolemic mini-swines.

Background: Postconditioning with multiple very short coronary occlusions immediately after prolonged ischemia has been found to reduce infarction size. However, it remains unknown whether postconditioning under the normal or hypercholesterolemic condition can also reduce myocardial no-reflow for which endothelial dysfunction is an important mechanism.

Methods: Twenty-four normal mini-swines were randomized into 3 study groups: 8 in control, 8 in postconditioning, 8 in sham-operated group.

Pretreatment with simvastatin reduces myocardial no-reflow by opening mitochondrial K(ATP) channel.

Background And Purpose: Simvastatin, a cholesterol-lowering agent, can protect against endothelial dysfunction. However, the effects of simvastatin treatment on the restoration of blood flow to ischemic myocardium are not known. This study sought to assess such effects of simvastatin on an experimental model of myocardial no-reflow and to explore possible mechanisms.

Pretreatment with fosinopril or valsartan reduces myocardial no-reflow after acute myocardial infarction and reperfusion.

Background: Both fosinopril and valsartan are effective in protecting endothelial function. We hypothesized that they may also reduce myocardial no-reflow. In addition, suppression of adenosine triphosphate-sensitive K (KATP) channel opening is an important mechanism for myocardial no-reflow.

Post-infarction treatment with simvastatin reduces myocardial no-reflow by opening of the KATP channel.

Unlabelled: Simvastatin can prevent cardiac remodelling after myocardial infarction, though the exact mechanisms are uncertain. Myocardial no-reflow is associated with progressive cardiac remodelling. However, it remains unknown whether post-infarction treatment with simvastatin can also reduce myocardial no-reflow for which suppression of adenosine triphosphate-sensitive K+ (K(ATP)) channel opening is an important mechanism.

Apolipoprotein B is associated with metabolic syndrome in Chinese families with familial combined hyperlipidemia, familial hypertriglyceridemia and familial hypercholesterolemia.

There is a paucity of data concerning the metabolic syndrome (MetS) in families with familial combined hyperlipidemia (FCHL), familial hypertriglyceridemia (FHTG), familial hypercholesterolemia (FH) and normolipidemic families in China. This study investigated the prevalence of MetS in these families and explored potential factors relevant to MetS. We recruited 70 families with 560 individuals > or = 20 years of age, including 43 FCHL families with 379 individuals, 3 FHTG families with 30 individuals, 16 FH families with 102 individuals and 8 normolipidemic families with 49 individuals.

Carvedilol preserves endothelial junctions and reduces myocardial no-reflow after acute myocardial infarction and reperfusion.

Introduction: Myocardial no-reflow, has been associated with alterations in endothelial junctions, which is regulated in part by endothelial dysfunction. Carvedilol is an alpha1 and nonselective beta-adrenergic receptor antagonist with antioxidative properties known to protect endothelial function. Therefore, we hypothesized that carvedilol might also have protective effects on myocardial no-reflow and endothelial junctions.

Nicorandil reduces myocardial no-reflow by protection of endothelial function via the activation of KATP channel.

Introduction: It has been found that nicorandil can attenuate myocardial no-reflow. However, the exact cause of this beneficial effect has remained unclear. We investigated whether the beneficial effect of nicorandil on myocardial no-reflow could be partly due to its protection against endothelial dysfunction.

Associations of apolipoprotein B with pulse pressure and glucose in Chinese families with familial combined hyperlipidemia.

Familial combined hyperlipidemia (FCHL), with a marked elevation of apolipoprotein B (apoB), is estimated to cause 10-20% of premature coronary artery disease. However, little data are available to demonstrate the associations of apoB with pulse pressure and glucose levels in FCHL families in China. This study was to investigate the potential influence factors for blood pressure and glucose phenotypes in FCHL families by multiple linear regression analysis.

Different effects of adenosine and calcium channel blockade on myocardial no-reflow after acute myocardial infarction and reperfusion.

Background: Adenosine and calcium channel blockers have been used in the treatment of angiographic no-reflow directly after angioplasty for acute myocardial infarction (AMI). However, their effects on tissue perfusion after AMI and reperfusion are undefined. The present study was designed to compare the effect of adenosine with that of the calcium channel blockers diltiazem and verapamil on myocardial no-reflow.