Chest Tightness With QR and ST-Segment Elevation in Lead V1.

This case report describes a patient in their 50s with a 2-month history of worsening chest tightness and dyspnea after COVID-19 infection.

Syncope with QT-interval prolongation and T-wave inversion in anterior and inferior leads: Foreboder of a life-threatening condition?

Even though patients with pulmonary embolism usually present with respiratory distress and tachycardia, the patient presented with syncope only. Typical ECG changes associated with PE include right axis deviation, right bundle-branch block, S1Q3T3 pattern, arrhythmia, nonspecific ST-segment changes, QR pattern in lead V1, Brugada ECG pattern, and T-wave inversions in the precordial leads. However, his electrocardiogram showed QT-interval prolongation and simultaneous T-wave inversions in the inferior and anterior leads. This ECG pattern is crucial for diagnosing PE. The patient underwent computed tomography-pulmonary angiography, which revealed pulmonary embolism. At the same time, these ECG changes should be differentiated from those of long QT syndrome, myocardial ischemia, Takotsubo cardiomyopathy, post-pacing T-wave memory, hypertrophic cardiomyopathy, and subarachnoid hemorrhage.

Rapid wide QRS tachycardia with an unknown cause.

One-to-one atrioventricular conduction during atrial flutter is one of the most severe life-threatening arrhythmias and is hemodynamically perilous. Rapid wide QRS tachycardia often not only occurs in patients with ventricular tachycardia but is also found in supraventricular tachycardia/atrial flutter with preexistent QRS prolongation, supraventricular tachycardia/atrial flutter with QRS prolongation caused by an IC antiarrhythmic drug, and supraventricular tachycardia/atrial flutter with preexcitation. Furthermore, atrial flutter with 1:1 AVC via an accessory pathway is an uncommon presentation of Wolff-Parkinson-White syndrome. We present a case of atrial flutter with 1:1 rapid AVC in the presence of Wolff-Parkinson-White syndrome. Physicians should be familiar with the rapid wide QRS complex ECG pattern associated with AFL with 1:1 AVC via an accessory pathway. Establishing the definitive diagnosis is essential for selecting an appropriate treatment strategy for improving outcomes.

Effects of endothelial progenitor cells transplantation on hyperlipidemia associated kidney damage in ApoE knockout mouse model.

BACKGROUND: Hyperlipidaemia causes kidney damage over the long term. We investigated the effect of the administration of endothelial progenitor cells (EPCs) on the progression of kidney damage in a mouse model of hyperlipidaemia. METHODS: Apolipoprotein E-knockout (ApoE-/-) mice were treated with a high-cholesterol diet after spleen resection. Twenty-four weeks later, the mice were divided into two groups and intravenously injected with PBS or EPCs. Six weeks later, the recruitment of EPCs to the kidney was monitored by immunofluorescence. The lipid, endothelial cell, and collagen contents in the kidney were evaluated by specific immunostaining. The protein expression levels of transforming growth factor-ß (TGF-ß), Smad2/3, and phospho-Smad3 (p-smad3) were detected by western blot analysis. RESULTS: ApoE-/- mice treated with a high-fat diet demonstrated glomerular lipid deposition, enlargement of the glomerular mesangial matrix, endothelial cell enlargement accompanied by vacuolar degeneration and an area of interstitial collagen in the kidney. Six weeks after EPC treatment, only a few EPCs were detected in the kidney tissues of ApoE-/- mice, mainly in the kidney interstitial area. No significant differences in TGF-ß, p-smad3 or smad2/3 expression were found between the PBS group and the EPC treatment group (TGF-ß expression, PBS group: 1.06 ± 0.09, EPC treatment group: 1.09 ± 0.17, P = 0.787; p-smad3/smad2/3 expression: PBS group: 1.11 ± 0.41, EPC treatment group: 1.05 ± 0.33, P = 0.861). CONCLUSIONS: Our findings demonstrate that hyperlipidaemia causes basement membrane thickening, glomerulosclerosis and the vascular degeneration of endothelial cells. The long-term administration of EPCs substantially has limited effect in the progression of kidney damage in a mouse model of hyperlipidaemia.

Optimal antithrombotic therapy in patients with atrial fibrillation following percutaneous coronary intervention: A systemic review and meta-analysis.

A challenge for antithrombotic treatment is patients who present with atrial fibrillation (AF) and acute coronary syndrome, particularly in patients who have undergone coronary percutaneous intervention with stenting (PCIS). In the present study, a total of nine observational trials published prior to July 2017 that investigated the effects of dual antiplatelet therapy (DAPT; aspirin + clopidogrel) and triple oral antithrombotic therapy (TOAT; DAPT + warfarin) among patients with AF concurrent to PCIS were collected from the Medline, Cochrane and Embase databases and conference proceedings of cardiology, gastroenterology and neurology meetings. A meta-analysis was performed using fixed- or random-effect models according to heterogeneity. The subgroups were also analyzed on the occurrence of major adverse cardiac events (MACE), stroke and bleeding events in the two treatment groups. Analysis of baseline characteristics indicated that there was no significant difference in the history of coexistent disease or conventional therapies between the DAPT and TOAT groups. The primary end point incidence was 2,588 patients in the DAPT group (n=13,773) and 871 patients in the TOAT group (n=5,262) following pooling of all nine trials. There was no statistically significant difference in the incidence of primary end points between the DAPT and TOAT groups. Odds ratio (OR)=0.96, 95% confidence interval (CI)=0.73-1.27, P=0.79, with heterogeneity between trials (I2=82%, P<0.00001). Subsequently, on subgroup analysis, the results indicated no increased risk of major bleeding or ischemic stroke in the DAPT or TOAT group. However, compared with the TOAT group, there was an apparent increased risk of MACE plus ischemic stroke in the DAPT group (OR=1.62, 95% CI=1.43-1.83, P<0.00001) with heterogeneity between trials (I2=70%, P=0.01). In conclusion, the present meta-analysis suggests that TOAT (aspirin + clopidogrel + warfarin) therapy for patients with AF concurrent to PCIS significantly reduced the risk of MACE and stroke compared with DAPT (aspirin + clopidogrel) therapy. Further randomized controlled clinical trials are required to confirm the efficacy of the optimal antithrombotic therapy in patients with AF following PCIS.

Oral N-acetylcysteine for prophylaxis of contrast-induced nephropathy in patients following coronary angioplasty: A meta-analysis.

It is acknowledged that contrast-induced nephropathy (CIN) is a common cause of acute renal insufficiency after cardiac catheterization and affects mortality and morbidity. To date, it is unknown whether oral N-acetylcysteine (NAC) is able to prevent contrast-induced nephropathy (CIN) in patients undergoing coronary angioplasty. A meta-analysis of randomized controlled trials was performed to assess the effects of NAC in the prevention of CIN in patients following coronary angioplasty. A total of 19 studies published prior to January 2015 that investigated the efficacy of oral NAC for the prevention of CIN were collected from Medline, Cochrane and Embase databases and conference proceedings from cardiology and nephrology meetings. The primary point of investigation was CIN, and the secondary points were renal failure requiring dialysis, mortality and length of hospitalization. The meta-analysis was performed using fixed- or random-effect models according to heterogeneity. Up to January 2015, 19 randomized placebo-controlled clinical trials met the inclusion criteria for the meta-analysis, including 4,514 patients. The pooled data showed that oral NAC did not reduce the CIN incidence [relative risk 0.84, 95% confidence interval (CI) 0.65-1.10; P=0.20], without heterogeneity among trials (I2=29%). Thus, the present meta-analysis suggests that oral NAC therapy is not effective as an alternative treatment to prevent CIN in patients following angioplasty. Further high quality randomized clinical controlled trials are required to confirm the usage and availability of this treatment.

Down-regulation of lncRNA KCNQ1OT1 protects against myocardial ischemia/reperfusion injury following acute myocardial infarction.

This study aimed to investigate the protective effects of long non-coding RNA KCNQ1OT1 against myocardial ischemia/reperfusion (I/R) injury following acute myocardial infarction, as well as its regulatory mechanism. We used the cardiac muscle H9c2 cells under condition of oxygen glucose deprivation followed by reperfusion (OGD/R) to induce myocardial I/R injury. Then H9C2 cells were transfected with si-NC, si-KCNQ1OT1, pc-NC, pc-KCNQ1OT1, si-AdipoR1 and si-AdipoR2, respectively. The myocardial cell viability and apoptosis were respectively detected. In addition, the expression levels of inflammatory factors, apoptosis-related proteins and p38 MAPK/NF-κB pathway-related proteins were detected. Besides, an inhibitor of p38 MAPK/NF-κB pathway SB203580 was used to treat cells to verify the relationship between KCNQ1OT1 and p38 MAPK/NF-κB pathway. The expression of KCNQ1OT1 was significantly up-regulated in OGD/R-induced myocardial H9C2 cells. The OGD/R-induced decreased cell viability and AdipoR1 expression could be reversed after suppression of KCNQ1OT1. In addition, suppression of KCNQ1OT1 reduced OGD/R-induced increased expressions of TNF-α, IL-6 and IL-1ß and OGD/R-induced increased cell apoptosis, which were reversed after knockdown of AdipoR1. Besides, suppression of KCNQ1OT1 significantly down-regulated the OGD/R-induced increased expression of p-p38 and p-NF-κB, which were also reversed after knockdown of AdipoR1. Moreover, SB203580, an inhibitor of p38 MAPK/NF-κB signal pathway, could further enhance the inhibitory effects of KCNQ1OT1 suppression on the expression of p-p38, TNF-α, IL-6, IL-1ß and p-NF-κB in OGD/R-induced myocardial H9C2 cells. Suppression of KCNQ1OT1 may prevent myocardial I/R injury following acute myocardial infarction via regulating AdipoR1 and involving in p38 MAPK/NF-κB signal pathway.

Resveratrol lowers blood pressure in spontaneously hypertensive rats via calcium-dependent endothelial NO production.

OBJECTIVE: Resveratrol, a polyphenol of natural compounds, has beneficial cardiovascular effects, many of which are mediated by nitric oxide (NO). Resveratrol increases intracellular calcium and activates AMP-activated protein kinase (AMPK), all of which could increase NO production. We hypothesized that resveratrol via a calcium-dependent NO production lowers blood pressure (BP) in spontaneously hypertensive rats (SHR). METHODS: Acetylcholine (Ach)-induced endothelium-dependent relaxations in rat aortas were examined by organ chamber. Blood pressures were determined by radiotelemetry methods. RESULTS: Incubation of isolated aortas from SHR with resveratrol dramatically improved vasorelaxation induced by Ach. Preincubation of aortas with endothelial NO synthase (eNOS) inhibitor or calcium chelant blunted the effects of resveratrol on Ach-induced relaxation, as wells as NO production and eNOS phosphorylation. In animal studies, administration of resveratrol significantly lowered systemic BP in SHR. CONCLUSION: Resveratrol increases endothelial NO production to improve endothelial dysfunction and lowers BP in hypertensive rats, which depends on calcium-eNOS activation.

Arsenic trioxide induces the apoptosis in vascular smooth muscle cells via increasing intracellular calcium and ROS formation.

The present study was designed to investigate whether arsenic trioxide induced the apoptosis in rat mesenteric arterial smooth muscle cells (SMCs), which provides new insights into mechanisms of arsenic-related vascular diseases. Here, we found that arsenic trioxide significantly decreased the viability of SMCs in a dose-dependent manner. In addition, higher level of arsenic trioxide directly caused cellular necrosis. The Hoechst and AO/EB staining demonstrated that apoptotic morphological change was presented in SMCs exposed to arsenic trioxide. The TUNEL assay displayed that more positive apoptotic signal appeared in SMCs treated with arsenic trioxide. The following result showed that ROS formation was markedly increased in arsenic trioxide-treated SMCs. Pretreatment with N-acetylcysteine, an anti-oxidant reagent, obviously attenuated the enhancement of ROS production and the reduction of cell viability induced by arsenic trioxide in SMCs. Arsenic trioxide also enhanced free intracellular Ca(2+) level in SMCs. BAPTA also significantly prevented the increased intracellular Ca(2+) and decreased cell viability induced by arsenic trioxide in SMCs. These results suggested that arsenic trioxide obviously induced apoptosis in SMCs, and its mechanism was partially associated with intracellular ROS formation and free Ca(2+) increasing.

Influence of the menstrual cycle on nonlinear properties of heart rate variability in young women.

This study was designed to assess the changes in nonlinear properties of heart rate (HR) variability (HRV) during the menstrual cycle by means of complexity measures, including sample entropy (SampEn) and correlation dimension (CD), and explore probable physiological interpretations for them. In 16 healthy women (mean age: 23.8 +/- 2.7 yr), complexity measures along with the spectral components of HRV (sympathovagal markers) were analyzed over 1,500 R-R intervals recorded during both the follicular phase (day 11.9 +/- 1.4) and the luteal phase (day 22.0 +/- 1.4) of each woman's menstrual cycle. Simultaneously, serum ovarian hormone (estradiol-17 and progesterone) and thyroid-related hormone [free triiodothyronine, free thyroxine (T(4)), and thyroid-stimulating hormone] concentrations were measured. With regard to HRV measures, SampEn, CD, and high-frequency (HF) components decreased from the follicular phase to the luteal phase, whereas normalized low-frequency (LF) components and the LF-to-HF ratio as well as resting HR increased. In regard to hormone levels, whereas progesterone was increased, the other hormone concentrations were unchanged. Furthermore, across the menstrual cycle, both SampEn and CD were well correlated with the spectral indexes and free T(4) concentrations, and SampEn also showed significant correlations with the ratio of estradiol-17 to progesterone concentrations. These results suggest that the nonlinear properties in HRV are altered during the regular menstrual cycle and that the autonomic nervous system, ovarian hormone balance, and free T(4) may be involved in nonlinear HR control in healthy women. All of these factors may enrich the physiological meanings of complexity measures.