Relation Between Calcium-Phosphorus Product and Total Coronary Artery Occlusion in a Nonchronic Kidney Disease Population: A Cross-Sectional Study.

Excessive calcium-phosphorus product (Ca-P product) in patients with chronic kidney disease (CKD) is associated with coronary artery calcification and coronary artery disease, but the relation between Ca-P product and coronary artery disease in non-CKD populations has rarely been reported. Therefore, we designed a cross-sectional study to investigate the role of Ca-P product in total coronary artery occlusion (TCAO) in a non-CKD population. We reviewed 983 patients who underwent coronary angiography at Guangyuan Central Hospital from February 2018 to January 2020. Ca-P product (mg2/dl2) was calculated as Ca (mmol/L) × 4 × P (mmol/L) × 3.1 and was analyzed as a continuous and tertiary variable. TCAO was defined as complete occlusion of any coronary artery by coronary angiography (thrombolysis in myocardial infarction flow grade 0). Statistical analysis was performed using univariate and multivariate logistic regression models and restricted cubic splines. Univariate logistic regression analysis showed a statistically significant association between Ca-P product and TCAO (odds ratio [OR] 0.97, 95% confidence interval [CI] 0.95 to 0.99, p <0.001). After stepwise adjustment for covariates, the risk of TCAO was reduced by 40% in the high versus low Ca-P group (OR 0.6, 95% CI 0.38 to 0.95, p = 0.031), and the risk of TCAO was predicted to decrease by 4% (OR 0.96, 95% CI 0.94 to 0.99, p = 0.006) for each unit increase in Ca-P product. Restricted cubic splines showed a nonlinear relation between Ca-P product and TCAO, with a significant decrease in the risk of TCAO after reaching 27.46 (nonlinear p = 0.047). In conclusion, in non-CKD populations, a higher Ca-P product (≥27.46 mg2/dl2) may help avoid TCAO.

Efficacy of Coronary Sinus Reducer in Patients With Non-revascularized Chronic Total Occlusions.

The coronary sinus reducer (CSR) has been introduced as therapy for patients with refractory angina with no other treatment options. Aim of this study is to investigate the efficacy of the CSR in patients with refractory angina and presence of coronary chronic total occlusions (CTO). In this multicentre, international retrospective study, patients undergoing CSR implantation were screened and divided in 2 groups according to the presence/absence of CTO lesions. Baseline and clinical characteristics were analyzed in the 2 groups. Primary-outcome consisted of the variation in Canadian Cardiovascular Society (CCS) class at 6-month follow-up. Between January 2014 and December 2018, 205 patients with refractory angina were consecutively treated with the study device in the participating centers, 103 (50.2%) of which had a CTO lesion at coronary angiogram and formed the CTO-group. Baseline characteristics of the study population were well balanced between the 2 groups. CSR was successfully implanted in all cases. Baseline CCS class was 3  ±  0.5 in the CTO-group versus 3.1  ±  0.6 in the non-CTO group (p = 0.45), and improved at follow-up to 1.6  ±  0.9 versus 2  ±  1.1 respectively (p <0.01), with a significantly higher improvement in CCS class in the CTO-group (1.4  ±  0.9 vs 1.1  ±  1 respectively, p = 0.01). Any improvement in CCS class was registered in 79 (80.6%) CTO-patients, while a significantly lower percentage (65 patients, 66.3%) of the non-CTO patients reported benefits in CCS class (p = 0.03). In conclusions, patients suffering from refractory angina with non-revascularized CTO lesions have a better response to CSR implantation than patients without CTOs. CSR implantation should be considered a valid complementary therapy to CTO-PCI in these patients.

Síndrome de la arteria de Percheron / Percheron artery syndrome

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Cardioprotective effect of polydatin on ventricular remodeling after myocardial infarction in coronary artery ligation rats.

The purpose of this study was to explore the effect of polydatin on ventricular remodeling after myocardial infarction in coronary artery ligation rats and to elucidate the underlying mechanisms. A rat model of ventricular remodeling after myocardial infarction was established by left coronary artery ligation. Rats with coronary artery ligation were randomly divided into five groups: control, plus 40 mg/kg captopril, plus 25 mg/kg polydatin, plus 50 mg/kg polydatin, and plus 100 mg/kg polydatin. The sham-operated group was used as a negative control. Rats were administered intragastrically with the corresponding drugs or drinking water for seven weeks. At the end of the treatment, the left ventricular weight index and heart weight index were assessed. The cross-sectional size of cardiomyocytes was measured by staining myocardium tissue with hematoxylin and eosin. Collagen content was counted by Sirius red in aqueous saturated picric acid. The concentrations of angiotensin I, angiotensin II, aldosterone, and endothelin 1 in myocardium or serum were determined by radioimmunoassay. Hydroxyproline and nitric oxide concentrations and glutathione peroxidase and catalase activities in serum were measured by ultraviolet spectrophotometry. Our results showed that seven weeks of polydatin treatment resulted in a significantly reduced left ventricular weight index, heart weight index, serum concentrations of hydroxyproline and aldosterone, an increased concentration of nitric oxide as well as enhanced activities of glutathione peroxidase and catalase. Myocardial angiotensin I, angiotensin II, and endothelin 1 levels were also reduced. The cardiomyocyte cross-sectional area and collagen deposition diminished. This study suggests that polydatin may attenuate ventricular remodeling after myocardial infarction in coronary artery ligation rats through restricting the excessive activation of the renin-angiotensin-aldosterone system and inhibiting peroxidation.

Preventive effect of yuzu and hesperidin on left ventricular remodeling and dysfunction in rat permanent left anterior descending coronary artery occlusion model.

Left ventricular (LV) remodeling, which includes ventricular dilatation and increased interstitial fibrosis after myocardial infarction (MI), is the critical process underlying the progression to heart failure. Therefore, a novel approach for preventing LV remodeling after MI is highly desirable. Yuzu is a citrus plant originating in East Asia, and has a number of cardioprotective properties such as hesperidin. However, no study has proved whether yuzu can prevent LV remodeling. The aim of this study was to determine the effects of yuzu on heart failure (HF) and its potential impact on the LV remodeling process after MI. Our in vivo study using the permanent left anterior descending coronary artery (LAD) occlusion model demonstrate that one week pre-treatment with yuzu or its major metabolite hesperidin before LAD occlusion significantly attenuated cardiac dysfunction, myocyte apoptosis and inflammation. Not only yuzu but also hesperidin inhibited caspase-3 activity, myeloperoxidase expression, α-smooth muscle actin expression, and matrix metalloproteinase-2 activity in a permanent LAD occlusion rat model. To our knowledge, our findings provide the first evidence that yuzu and hesperidin prevent MI-induced ventricular dysfunction and structural remodeling of myocardium.

Impact of a chronic total occlusion in an infarct-related artery on the long-term outcome of ventricular tachycardia ablation.

INTRODUCTION: In patients with a prior myocardial infarction (MI), angiographic predictors of ventricular tachycardia (VT) recurrence after ablation are lacking. Recently, a proarrhythmic effect of a chronic total occlusion (CTO) in a coronary artery has been suggested. METHODS AND RESULTS: A total of 191 patients with prior MI were referred to our Hospital between 2010 and June 2013 for a first ablation of VT. Of these, 84 patients (44%) with stable coronary artery disease that underwent a coronary angiography during the index hospitalization were included in this study. A CTO in an infarct-related artery (IRA-CTO) was present in 47 patients (56%). Patients with and without IRA-CTO did not differ in terms of comorbidities, severity of heart failure, presentation of VT or acute outcome of ablation, that was completely successful in 93% of cases. At electroanatomic mapping, IRA-CTO was associated with greater scar and especially with greater area of border zone (34 cm(2) vs. 19 cm(2) , P = 0.001). Median follow-up was 19 months (IQR 18). At follow-up, patients with IRA-CTO had a significantly higher rate of VT recurrence (47% vs. 16%, P = 0.003). At multivariate analysis, IRA-CTO resulted to be an independent predictor of VT recurrence after ablation (HR 4.05, P = 0.004). CONCLUSIONS: IRA-CTO is an independent predictor of VT recurrence after ablation and identifies a subgroup of patients with high recurrence rate despite a successful procedure. IRA-CTO is associated with greater scars and border zone area; however, this association does not completely justify its proarrhythmic effect.

Esmolol activates endogenous neurokinin activity inhibiting infarction-induced arrhythmias in rats: novel mechanisms of anti-arrhythmia.

Endogenous neurokinin and adrenergic mechanisms might co-participate in the pathology of acute myocardial infarction (MI). This study sought to investigate the role of endogenous neurokinin and its relationship with ß1-adrenergic mechanism in the infarction induced arrhythmias. In 60min of MI in rats, the contents of substance P (SP), a native agonist of neurokinin 1 receptor (NK1-R), norepinephrine (NE), NK1-R and ß1-adrenergic receptor in the myocardium at risk of ischemia were examined and the ventricular arrhythmias were analyzed. The effects of pretreatment with D-SP (152ng/kg), a specific antagonist of NK1-R, esmolol (10mg/kg), a specific blocker of ß1-adrenergic receptor, and a combination of the two blockers were studied. The results showed that the overlaps of up-regulation of NE, SP and the increase of ventricular arrhythmias were observed. D-SP exacerbated the episodes and duration of VT & VF by 54% and 104%, respectively (all P<0.05). Esmolol inhibited the morbidity rate, the episodes and the duration of VT & VF by 66%, 92% and 95%, respectively. Surprisingly, esmolol significantly attenuated the arrhythmogenic effect of D-SP throughout the MI, beyond the time span of esmolol action, during which a significant up-regulation of the NK1-R (by 19%, P<0.05) was detected. In conclusion, the findings of this study may indicate an anti-arrhythmic effect of endogenous neurokinin mechanism, through the activation of which, via up-regulation of NK1 receptor, esmolol may exert its anti-arrhythmic action at the early time of acute myocardial infarction.

In vive and in vitro cardioprotective effects of panax quinquefolium 20(S)-protopanaxadiol saponins (PQDS), isolated from panax quinquefolium.

In this study, we investigated the cardioprotective effect of Panax quinquefolium 20(S)-protopanaxadiol saponins (PQDS) both in vivo and in vitro. An animal model of acute myocardial infarction was induced by permanent ligation of the left anterior descending coronary artery in Sparague Dawley rats. Neonatal rat cardiomycocytes were used to examine the cytoprotective effect of PQDS against H202 exposure. Pretreatment with PQDS (25 and 50 mg/kg) could significantly improve the heart function, remarkably decrease infarct size from 20.87% to 14.87% (p<0.01), decrease the levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and cardiac troponin T (cTnT) content in serum (p< 0.05). Meanwhile, pretreatment with PQDS (25 and 50 mg/kg) significantly increased the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-Px) in the heart, and decreased the level of malondiadehyde (MDA) in the myocardium (p<0.05). Histopathological results demonstrated the same protective effect of PQDS. Pretreatment with PQDS (200 and 400 microg/ml) prior to H202 exposure could increase cell viability of neonatal rat cardiomycocytes. Pretreatment PQDS (200 and 400 microg/ml) also increased the activity of SOD, decreased level of LDH in the cultured supernatant and the MDA level in cardiomyocytes. These results indicated that PQDS had a cardioprotective effect proven in vivo and in vitro. The mechanisms might be due to its scavenging lipid peroxidation products, increasing endogenous antioxidant defense enzymes.

Antiarrhythmic properties of long-term treatment with matrine in arrhythmic rat induced by coronary ligation.

Matrine, a monomer of traditional Chinese medicine Sophora flavescens, is a potential drug for treatment of arrhythmia. The aim of the study is to elucidate the protective effects of matrine on arrhythmic rat induced by myocardial infarction (MI) and further explore underlying targets. Experiments were performed to investigate the effects of long-term oral administration of matrine on coronary ligation induced arrhythmia, measured in whole animals, via surface electrocardiogram (ECG). Whole-cell patch-clamp technique was used to record the action potential and potassium ionic currents in myocytes isolated from rat hearts. The cytoplasmic free Ca(2+) concentration ([Ca(2+)](i)) was measured using the scanning confocal microscopy. Mortality rate was 19/30 (63%) in MI group and 10/30 (33%) in matrine group (p<0.05). This represented a 1.9-fold reduction in long-term mortality rate. The prolonged action potential duration (APD) induced by MI were significantly shortened by long-term treatment of matrine. Matrine restored Kv4.2/I(to), Kir2.1/I(K1) in rat ventricular myocytes after MI. Abnormaly decreased [Ca(2+)](i) mediated by ischemia can be recovered by matrine. Our results suggested that long-term oral administration of matrine reduced arrhythmia and mortality. Electrophysiological experiment revealed that long-term matrine treatment played an important role in anti-arrhythmia through ionic mechanism. Knowledge of matrine from this work may provide insight into the development of new drugs for long-term myocardial infarction treatment.

Hyperbaric oxygenation applied immediately after coronary occlusion reduces myocardial necrosis and acute mortality in rats.

1. Because in ischaemia there is a critical lack of O2, it has been reasoned that increasing O2 delivery to the ischaemic myocardium could serve as adjunctive therapy for acute myocardial infarction (MI). Accordingly, in the present study, the effect of early hyperbaric oxygenation (HBO) on mortality and MI size after coronary occlusion was examined in rats. 2. After coronary occlusion, male Wistar rats were randomly assigned to receive either HBO for 1 h in a hyperbaric chamber (100% O(2) at 253 kPa; n = 106) or ambient O2 as the control (n = 111). The extent of myocardial necrosis was assessed (triphenyltetrazolium) immediately after treatment in the HBO (n = 50) and control (n = 47) groups. The remaining rats were evaluated 24 h after occlusion to enable calculation of MI size and mortality. 3. Immediately after therapy, the size of the MI was significantly greater in the control group compared with that in the HBO group (40 +/- 3 vs 27 +/- 2% of the left ventricle (LV), respectively; P < 0.001). The 24 h mortality of control rats was higher than that of HBO rats (34 vs 16%, respectively; P = 0.02). Control rats that survived 24 h had a larger MI than did HBO rats that survived 24 h (40 +/- 4 vs 29 +/- 3% of the LV, respectively; P = 0.005). Furthermore, large necrotic areas (> 40% of the LV) were more frequent in control than HBO rats (55 vs 27% of infarcted hearts, respectively; P = 0.01). There was less pulmonary congestion observed in HBO rats compared with control rats. 4. In conclusion, early therapy with HBO during the onset of an acute ischaemic event decreases the necrotic area and reduces acute mortality. These data support further investigation of HBO as an adjuvant therapy for acute MI.