Mortality In Heart Disease Patients Research Articles

Sleep duration and mortality in patients with chronic noncommunicable disease: a population-based cohort study.

Inadequate sleep behaviors may confer a higher risk of premature death, however, evidence in patients with chronic noncommunicable disease (NCD) is scarce. To investigate the relationship between sleep duration and mortality from all-cause and heart diseases in NCD patients from a prospective cohort. Totally, 14,171 participants with at least one NCD, including 8275 with hypertension, 7547 with high cholesterol, 4065 with diabetes, and 5815 with chronic renal failure were enrolled from the National Health and Nutrition Examination Survey during 2005-2014. Cox proportional hazard models were performed to estimate the hazard ratio (HR) for sleep duration and mortality after adjusting for potential confounding factors. After a median follow-up of 9 years, 2514 all-cause deaths were identified. Compared with sleeping 7-8 h/day, sleeping over 8 h/day was significantly associated with a higher risk of all-cause mortality, where the multivariable-HRs were 1.29 (1.11, 1.50) for hypertension, 1.23 (1.01, 1.51) for high cholesterol, 1.44 (1.13, 1.82) for diabetes, and 1.36 (1.10, 1.68) for chronic renal failure. Similar patterns were observed for heart disease mortality. A nonlinear association was detected between sleep duration and mortality in patients with NCD. Age modified the association in patients with hypertension (P-interaction: 0.036). Trouble sleeping modified the association in patients with diabetes (P-interaction: 0.042). Long sleep duration was associated with higher risks of all-cause and heart disease mortality in patients with chronic NCD. Our findings highlight that improving sleep behaviors may decrease the risk of premature deaths and help to NCD tertiary prevention.

Viral Transgene Expression in Rodent Hearts and the Assessment of Cardiac Arrhythmia Risk.

Heart disease is the leading cause of morbidity and mortality worldwide. Due to their low cost, ease of handling, and abundance of transgenic strains, rodents have become essential models for cardiovascular research. However, spontaneous lethal cardiac arrhythmias that often cause mortality in heart disease patients are rare in rodent models of heart disease. This is primarily due to the species differences in cardiac electrical properties between humanand rodents and poses a challenge to the study of cardiac arrhythmias using rodents. This protocol describes an approach to enable efficient transgene expression in mouse and rat ventricular myocardium using echocardiography-guided intramuscular injections of recombinant virus (adenovirus and adeno-associated virus). This work also outlines a method to enable reliable assessment of cardiac susceptibility to arrhythmias using isolated, Langendorff-perfused mouse and rat hearts with both adrenergic and programmed electrical stimulations. These techniques are critical for studying heart rhythm disorders associated with adverse cardiac remodeling after injuries, such as myocardial infarction.

Good Physician Adherence to Guideline-Directed Medical Therapy Associated with Lower Patient Mortality and Hospitalisation Rates Across The World

While the guidelines for the managements of heart diseases have been well-developed and updated periodically, they do not guarantee to reduce the number of heart disease morbidity and mortality. Since the holistic approach is not carefully applied, this morbidity rate may not be significantly reduced. The holistic approach to managing heart disease has broad aspects, but the most important aspect is regarding physician adherence to Guideline-Directed Medical Therapy (GDMT). This paper aimed to discuss the physician adherence to GDMT, and its role in reducing morbidity and in-hospitalization in heart disease patients. Several large scale studies have revealed that good adherence to heart failure treatment guidelines among physicians improved not only quality of life but also resulted in a better prognosis. On other hands, because the main target of physicians adherence to GDMT is to achieve maximally tolerated dose, it is also important that the understanding when and how to add, switch, and titrate all therapies to maximally tolerated doses and ideally target doses is important to reduce the morbidity and mortality of heart disease patients. However, in some points, this principle might not be applied properly due to several limitations. In this case, physicians may have to consider the balance between patients preferences, healthcare resources, and the risk of adverse outcomes. In conclusion, it should be noted that physician adherence to GDMT has an important role to reduce morbidity and mortality of heart disease patients.

LCZ696, an Angiotensin Receptor-Neprilysin Inhibitor, Improves Cardiac Hypertrophy and Fibrosis and Cardiac Lymphatic Remodeling in Transverse Aortic Constriction Model Mice.

Cardiac hypertrophy and ventricular remodeling following heart failure are important causes of high mortality in heart disease patients. The cardiac lymphatic system has been associated with limited research, but it plays an important role in the improvement of myocardial edema and the promotion of fluid balance. LCZ696 is a novel combination of angiotensin and neprilysin inhibitors. Here, we studied the role played by LCZ696 during transverse aortic constriction (TAC) induced cardiac hypertrophy and changes in the lymphatic system. Mice undergoing aortic coarctation were constructed to represent a cardiac hypertrophy model and then divided into random groups that either received treatment with LCZ696 (60 mg/kg/d) or no treatment. Cardiac ultrasonography was used to detect cardiac function, and hematoxylin and eosin (H&E) and Masson staining were used to detect myocardial hypertrophy and fibrosis. The proinflammatory factors interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α) were detected in the blood and heart tissues of mice. The protein expression levels of lymphatic-specific markers, such as vascular endothelial growth factor C (VEGF-C), VEGF receptor 3 (VEGFR3), and lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) were detected in mouse heart tissues. We also examined the colocalization of lymphatic vessels and macrophages by immunofluorescence. The results showed that LCZ696 significantly improved heart dysfunction, cardiac hypertrophy, and fibrosis and inhibited the expression of proinflammatory factors IL-6, IL-1β, and TNF-α in the circulating blood and heart tissues of mice. LCZ696 also decreased the protein expression levels of VEGF-C, VEGFR3, and LYVE-1 in mouse heart tissues, ameliorated the transport load of lymphatic vessels to macrophages, and improved the remodeling of the lymphatic system in the hypertrophic cardiomyopathy model induced by TAC.

Novel Insights into the Crosstalk between Mineralocorticoid Receptor and G Protein-Coupled Receptors in Heart Adverse Remodeling and Disease

The mineralocorticoid hormone aldosterone regulates sodium and potassium homeostasis but also adversely modulates the maladaptive process of cardiac adverse remodeling post-myocardial infarction. Through activation of its mineralocorticoid receptor (MR), a classic steroid hormone receptor/transcription factor, aldosterone promotes inflammation and fibrosis of the heart, the vasculature, and the kidneys. This is why MR antagonists reduce morbidity and mortality of heart disease patients and are part of the mainstay pharmacotherapy of advanced human heart failure. A plethora of animal studies using cell type–specific targeting of the MR gene have established the importance of MR signaling and function in cardiac myocytes, vascular endothelial and smooth muscle cells, renal cells, and macrophages. In terms of its signaling properties, the MR is distinct from nuclear receptors in that it has, in reality, two physiological hormonal agonists: not only aldosterone but also cortisol. In fact, in several tissues, including in the myocardium, cortisol is the primary hormone activating the MR. There is a considerable amount of evidence indicating that the effects of the MR in each tissue expressing it depend on tissue- and ligand-specific engagement of molecular co-regulators that either activate or suppress its transcriptional activity. Identification of these co-regulators for every ligand that interacts with the MR in the heart (and in other tissues) is of utmost importance therapeutically, since it can not only help elucidate fully the pathophysiological ramifications of the cardiac MR’s actions, but also help design and develop novel better MR antagonist drugs for heart disease therapy. Among the various proteins the MR interacts with are molecules involved in cardiac G protein-coupled receptor (GPCR) signaling. This results in a significant amount of crosstalk between GPCRs and the MR, which can affect the latter’s activity dramatically in the heart and in other cardiovascular tissues. This review summarizes the current experimental evidence for this GPCR-MR crosstalk in the heart and discusses its pathophysiological implications for cardiac adverse remodeling as well as for heart disease therapy. Novel findings revealing non-conventional roles of GPCR signaling molecules, specifically of GPCR-kinase (GRK)-5, in cardiac MR regulation are also highlighted.

Neutrophil to lymphocyte ratio as a predictor of myocardial damage and cardiac dysfunction in acute coronary syndrome patients

BackgroundNeutrophil to lymphocyte ratio (NLR) in peripheral blood is established to correlate with the morbidity and mortality of heart disease patients. We aimed to define the severity of inflammation (NLR) by observing the association of NLR with cardiac functions or myocardial damage parameters in patients with acute myocardial infarction. MethodsData from 715 patients who underwent percutaneous coronary intervention (PCI) within 72hours of incidence in 2016 were analysed retrospectively. ResultsThe NLR ranges from 0.50 to 46 (medium±SD, 2.76±2.96) in 715 patients. NLR positively correlated with myocardial damage (NLR vs. CK-mB: p<0.0001) but negatively correlated with myocardial function (NLR vs. EF: p<0.0001; NLR vs. FS: p<0.0001). Myocardial damage markers (CK, CK-mB, ASL, LDH) were significantly increased, and cardiac contractile parameters (EF and FS) were reduced at NLR>2.76 compared to those of NLR<2.76. ELISA analysis has shown that IL-10 was significantly increased when NLR≥4.6 and TGF-β was increased at NLR>4. The correlation was diminished between NLR and CK-mB at NLR>2.76 or at NLR>4, but that of NLR and EF or FS was maintained in NLR>2.76 and at NLR>4. EF and FS were comparable between NLR>2.76 and NLR>4. But myocardial damage parameters increased significantly at NLR>4 compared to those of NLR>2.76. ConclusionNLR is a strong predictor of myocardial damage in acute myocardial patients. High NLR are associated with myocardial dysfunction in all the patients. Severe inflammation (NLR) can predict the consequence of the heart in patients with coronary syndrome.

Effects of Alcoholic Extract of Stem and Aerial Parts of the Alcea angulate Plant on Aorta Atherosclerotic Plaque Formation in Rabbit

Background: Atherosclerosis is the main cause of mortality in heart disease patients that its dependence on cholesterol levels has been shown. The side effects of chemical drugs have created a tendency toward medicinal plants for treatment of diseases. Objective: The aim of this study is to evaluate the effect of alcoholic extract of the Alcea angulate on the formation of atherosclerotic plaque due to hypercholesterolemia in rabbit aorta. Methods: 25 male New Zealand white rabbits were divided randomly into 5 groups. Two months respectively treated with basic diet [group 1], basic diet plus 1% cholesterol [control group, group 2], 1% cholesterol with diet intervention Alcea angular at doses of 200, 400 and 800 mg/kg of body weight [groups 3, 4 and 5]. Blood lipid profile levels were measured after 60 days. At the end of the study, the animals were scarified and lipid profile and atherosclerotic plaque formation in the aorta arteries was measured. Data using SPSS ver. 16 were analyzed. Tukey HSD test was used to compare paired groups. Results: Serum levels of total cholesterol and LDL.C of the groups which treated with the Alcea angulata was significantly lower than the control group (p<0.01). Serum levels of HDL in treated groups compared to the control group significantly increased (p<0.01). Pathology studies showed the desired effects and mitigation of extract on the progression of aorta atherosclerosis in hypercholesterolemic rabbits. Conclusion: The overall result demonstrated that use of the Alcea angulate plant reduced total cholesterol and LDL in the blood and inhibited the atherosclerotic plaque formation.

Stem cell therapies may reduce mortality in heart disease patients

Stem cell therapies may reduce mortality in heart disease patients

Comparison Of Heart Rate Variability Methods During Incremental And Ramped Cycling Exercise In Healthy Males

Heart rate variability (HRV) is recognised as a predictor of all-cause mortality in heart disease patients and as a measure of the autonomic nervous system. Previous investigations suggest HRV may be a measure of parasympathetic activity during exercise and an alternative method for determination of exercise thresholds. In order to apply this to the accurate detection of changes over time, the underlying variability must first be established. PURPOSE: To investigate the reproducibility of 2 contemporary HRV measures; root mean square of successive difference measured in 30 second blocks (rMSSD30) and Short Time Fourier Transform (STFT) during graded cycling exercise. Method: Fifteen male participants (24 ±5 years) completed 2 incremental and 2 ramped cycling protocols to assess steady and non-steady physiological states. Tests were randomised for protocol and order. The incremental test started at 0 watts with 36 watt increases every 3 minutes, and the ramp protocol started at 0 watts with a 1 watt increase every 5 seconds up to 85% of each participants age predicted maximum heart rate. HRV variables were processed in 30 second averages with the final 30 seconds of each 3minute increment analysed. STFT was processed with either a 256 or 512 sample window to determine power spectral density (PSD) at low (PSDLF 256 or PSDLF 512) and high frequencies (PSDHF 256 or PSDHF 512) and high frequency peak (HFpk 256 or HFpk 512). Overall reliability was determined using % coefficient of variation (CV) and Intra-class correlation coefficients (ICC) across all workloads. RESULTS: For the ramp protocol CV was lower for all variables. HFpk was the most reliable HRV variable and HFpk 512 displayed lower CV and higher ICC (26% & 0.63) than HFpk 256 (28% & 0.45). Results for rMSSD30 were; 48% & 0.7 and 50% & 0.7 (CV & ICC) for ramp and incremental respectively. All PSD measures had CV exceeding 100%. CONCLUSION: All measures displayed high test-retest variability. STFT HFpk was the most consistent HRV measure during exercise and this showed further improvement with a ramp protocol and 512 sample window. The low reproducibility of these measures overall, suggests that HRV measures during exercise may not be suitable to detect change over time, or for diagnostic or prescriptive purposes.

High-Sensitivity C-Reactive Protein and Coronary Heart Disease Mortality in Patients With Type 2 Diabetes

To investigate in a follow-up study whether high-sensitivity C-reactive protein (hs-CRP) predicts coronary heart disease (CHD) events in subjects with type 2 diabetes. The original study population consisted of 1,059 patients with type 2 diabetes (age 45-64 years). Mean duration of diabetes was 8 years. CRP values were available from 1,045 subjects, of whom 878 were free of myocardial infarction (MI) at baseline. CHD mortality and the incidence of nonfatal MI were assessed in a 7-year follow-up. Altogether, 157 patients died from CHD and 254 had a nonfatal or fatal CHD event. Patients with hs-CRP >3 mg/l had a higher risk for CHD death than patients with hs-CRP < or =3 mg/l (19.8 and 12.9%, respectively, P = 0.004). In Cox regression analysis, patients with high hs-CRP had a relative risk of 1.72 for CHD death even after the adjustment for confounding factors (P = 0.002). Among subjects who were free from MI at baseline, those with a high hs-CRP level had relative risks of 1.83 (P = 0.003) and 1.84 (P = 0.004) for CHD death in univariate and multivariate analyses, respectively. In this large cohort of type 2 diabetic patients, hs-CRP was an independent risk factor for CHD deaths.

White Blood Cell Count Predicts Reduction in Coronary Heart Disease Mortality With Pravastatin

Elevated serum inflammatory marker levels are associated with a greater long-term risk of cardiovascular events. Because 3-hydroxy-3-methylglutaryl coenzyme-A reductase inhibitors (statins) may have an antiinflammatory action, it has been suggested that patients with elevated inflammatory marker levels may have a greater reduction in cardiovascular risk with statin treatment. We evaluated the association between the white blood cell count (WBC) and coronary heart disease mortality during a mean follow-up of 6.0 years in the Long-Term Intervention With Pravastatin in Ischemic Disease (LIPID) Study, a clinical trial comparing pravastatin (40 mg/d) with a placebo in 9014 stable patients with previous myocardial infarction or unstable angina. An increase in baseline WBC was associated with greater coronary heart disease mortality in patients randomized to placebo (hazard ratio for 1x10(9)/L increase in WBC, 1.18; 95% CI, 1.12 to 1.25; P<0.001) but not pravastatin (hazard ratio, 1.02; 95% CI, 0.96 to 1.09; P=0.56; P for interaction=0.004). The numbers of coronary heart disease deaths prevented per 1000 patients treated with pravastatin were 0, 9, 30, and 38 for baseline WBC quartiles of <5.9, 6.0 to 6.9, 7.0 to 8.1, and >8.2x10(9)/L, respectively. WBC was a stronger predictor of this treatment benefit than the ratio of total to high-density lipoprotein cholesterol and a global measure of cardiac risk. There was also a greater reduction (P=0.052) in the combined incidence of cardiovascular mortality, nonfatal myocardial infarction, and stroke with pravastatin as baseline WBC increased (by quartile: 3, 41, 61, and 60 events prevented per 1000 patients treated, respectively). These data support the hypothesis that individuals with evidence of inflammation may obtain a greater benefit from statin therapy.