Reviews and Notes: Cardiology: Atlas of Heart Diseases. Vol. 4: Heart Failure

1996 ◽  
Vol 125 (6) ◽  
pp. 528
Author(s):  
Thomas D. Giles
Keyword(s):  
Heart Failure ◽  
Heart Diseases

Potential Role of Inflammation in Associations between Particulate Matter and Heart Failure

2018 ◽  
Vol 24 (3) ◽  
pp. 341-358 ◽  
Author(s):  
Xiaotong Ji ◽  
Yingying Zhang ◽  
Guangke Li ◽  
Nan Sang
Keyword(s):  
Heart Failure ◽  
Particulate Matter ◽  
Inflammatory Response ◽  
Heart Diseases ◽  
Experimental Studies ◽  
Epidemiological Studies ◽  
Inflammatory Mechanism ◽  
High Concentrations ◽  
Future Work ◽  
The Relationship

Recently, numerous studies have found that particulate matter (PM) exposure is correlated with increased hospitalization and mortality from heart failure (HF). In addition to problems with circulation, HF patients often display high expression of cytokines in the failing heart. Thus, as a recurring heart problem, HF is thought to be a disorder characterized in part by the inflammatory response. In this review, we intend to discuss the relationship between PM exposure and HF that is based on inflammatory mechanism and to provide a comprehensive, updated evaluation of the related studies. Epidemiological studies on PM-induced heart diseases are focused on high concentrations of PM, high pollutant load exposure in winter, or susceptible groups with heart diseases, etc. Furthermore, it appears that the relationship between fine or ultrafine PM and HF is stronger than that between HF and coarse PM. However, fewer studies paid attention to PM components. As for experimental studies, it is worth noting that coarse PM may indirectly promote the inflammatory response in the heart through systematic circulation of cytokines produced primarily in the lungs, while ultrafine PM and its components can enter circulation and further induce inflammation directly in the heart. In terms of PM exposure and enhanced inflammation during the pathogenesis of HF, this article reviews the following mechanisms: hemodynamics, oxidative stress, Toll-like receptors (TLRs) and epigenetic regulation. However, many problems are still unsolved, and future work will be needed to clarify the complex biologic mechanisms and to identify the specific components of PM responsible for adverse effects on heart health.

Carvedilol Inhibits Matrix Metalloproteinase-2 Activation in Experimental Autoimmune Myocarditis: Possibilities of Cardioprotective Application

2017 ◽  
Vol 23 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Monika Skrzypiec-Spring ◽  
Katarzyna Haczkiewicz ◽  
Agnieszka Sapa ◽  
Tomasz Piasecki ◽  
Joanna Kwiatkowska ◽  
...  
Keyword(s):  
Heart Failure ◽  
Troponin I ◽  
Heart Function ◽  
Heart Diseases ◽  
Acute Myocarditis ◽  
Study Groups ◽  
Matrix Metalloproteinase 2 ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

Aims: Acute myocarditis is a potentially lethal inflammatory heart disease that frequently precedes the development of dilated cardiomyopathy and subsequent heart failure. At present, there is no effective standardized therapy for acute myocarditis, besides the optimal care of heart failure and arrhythmias in accordance with evidence-based guidelines and specific etiology-driven therapy for infectious myocarditis. Carvedilol has been shown to be cardioprotective by reducing cardiac pro-inflammatory cytokines present in oxidative stress in certain heart diseases. However, effects of carvedilol administration in acute myocarditis with its impact on matrix metalloproteinases’ (MMPs) activation have not been elucidated. Methods and Results: Carvedilol in 3 doses (2, 10, and 30 mg/kg) was given daily to 3 study groups of rats (n = 8) with experimental autoimmune myocarditis by gastric gavage for 3 weeks. In comparison to untreated rats (n = 8) with induced myocarditis, carvedilol significantly prevented the left ventricle enlargement and/or systolic dysfunction depending on the dose in study groups. Performed zymography showed enhanced MMP-2 activity in untreated rats, while carvedilol administration reduced alterations. This was accompanied by prevention of troponin I release and myofilaments degradation in cardiac muscle tissue. Additionally, severe inflammatory cell infiltration was detected in the nontreated group. Carvedilol in all doses tested, had no impact on severity of inflammation. The severity of inflammation did not differ between study groups and in relation to the untreated group. Conclusions: The protective effects of carvedilol on heart function observed in the acute phase of experimental autoimmune myocarditis seem to be associated with its ability to decrease MMP-2 activity and subsequently prevent degradation of myofilaments and release of troponin I while not related to suppression of inflammation.

scholarly journals mtDNA in the Pathogenesis of Cardiovascular Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Lili Wang ◽  
Qianhui Zhang ◽  
Kexin Yuan ◽  
Jing Yuan
Keyword(s):  
Heart Failure ◽  
Cardiovascular Disease ◽  
Mitochondrial Dna ◽  
Copy Number ◽  
Heart Diseases ◽  
Mtdna Copy Number ◽  
Cardiac Inflammation ◽  
Ischemic Heart Diseases ◽  
Metabolic Functions ◽  
Underlying Mechanisms

The incidence rate of cardiovascular disease (CVD) has been increasing year by year and has become the main cause for the increase of mortality. Mitochondrial DNA (mtDNA) plays a crucial role in the pathogenesis of CVD, especially in heart failure and ischemic heart diseases. With the deepening of research, more and more evidence showed that mtDNA is related to the occurrence and development of CVD. Current studies mainly focus on how mtDNA copy number, an indirect biomarker of mitochondrial function, contributes to CVD and its underlying mechanisms including mtDNA autophagy, the effect of mtDNA on cardiac inflammation, and related metabolic functions. However, no relevant studies have been conducted yet. In this paper, we combed the current research status of the mechanism related to the influence of mtDNA on the occurrence, development, and prognosis of CVD, so as to find whether these mechanisms have something in common, or is there a correlation between each mechanism for the development of CVD?

scholarly journals Mortality Sensitivity of Cardiovascular, Cerebrovascular, and Respiratory Diseases to Warm Season Climate in Japanese Cities

Atmosphere ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1546
Author(s):  
Yukitaka Ohashi ◽  
Akari Miyata ◽  
Tomohiko Ihara
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Respiratory Diseases ◽  
Heart Diseases ◽  
Warm Season ◽  
Respiratory Mortality ◽  
Ischemic Heart Diseases ◽  
Mean Temperature ◽  
Risk Ratios

We investigated decadal (2010–2019) cardiovascular, cerebrovascular, and respiratory mortality sensitivity to annual warm temperatures in major Japanese cities: Sapporo, Tokyo (23 wards), and Osaka. The summer mortalities (June–August) increased with the monthly mean temperature for acute myocardial infarction, other acute ischemic heart diseases, cerebral infarction, and pneumonia in the three cities. Monthly mean temperatures were an indicator of these disease mortalities in Japan. However, similar responses were not found for cardiac arrhythmia and heart failure (excluding Sapporo), subarachnoid hemorrhage, and intracerebral hemorrhage. The decadal sensitivities and risk ratios between the maximum and minimum monthly mean temperatures were calculated using a linear regression model. In Sapporo, Tokyo, and Osaka, for example, the analyses of acute myocardial infarction showed summer positive responses of 0.19–0.25, 0.13–0.18, and 0.12–0.30, respectively, as the mortality rate (per 100,000 population) per 1 °C of monthly mean temperature, which estimated increased risks (between the coolest and hottest months) of 37–65% in Sapporo, 31–42% in Tokyo, and 35–39% in Osaka.

scholarly journals A CRITICAL REVIEW AND LOCAL AUDIT OF THE PREVALENCE OF MENTAL ILL-HEALTH IN HEART FAILURE PATIENTS

2020 ◽  
pp. 10-16
Author(s):  
MARIAM AHMED ◽  
HANA MORRISSEY ◽  
PATRICK ANTHONY BALL
Keyword(s):  
Heart Failure ◽  
Heart Diseases ◽  
Local Population ◽  
Population Data ◽  
Management Plan ◽  
Local Data ◽  
Heart Failure Patients ◽  
Cardiac Outcomes ◽  
Artery Disease ◽  
Two Phases

Objective: To establish if depression results in poor adherence to therapy in patients with heart diseases. Methods: This concept scoping study was conducted in two phases; the first was a systematic review of the literature, and the second part was local data analysis. Statistical analysis was performed using RevMan® V.5.3 (Cochrane Community). Results: Patients who received multidisciplinary collaborative care showed significantly reduced major adverse cardiac outcomes in patients with cardiovascular diseases. They also demonstrated higher rates of self-reported remission of depression. The review also showed endpoint mortality after PCI was associated with patients having depression. Local population data showed that 26% of heart failure patients had mental ill health comorbidity, however, only 12% had a formal diagnosis recorded. Conclusion: Depression is associated with poor cardiac outcomes in patients with coronary artery disease. It is widespread in patients with cardiovascular disease and must be screened for throughout the management plan.

Abstract 19292: KLF4 Regulates Mitochondrial Homeostasis in the Heart

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Xudong Liao ◽  
Mukesh Jain
Keyword(s):  
Heart Failure ◽  
Mitochondrial Biogenesis ◽  
Transcriptional Control ◽  
Heart Function ◽  
Heart Diseases ◽  
Pressure Overload ◽  
Premature Mortality ◽  
Mitochondrial Homeostasis ◽  
Adult Mice ◽  
Mitochondrial Heterogeneity

Mitochondrial homeostasis is critical for heart function and mitochondrial dysfunction contributes to numerous heart diseases such as heart failure. Our previous work indicates that mice with cardiomyocyte-restricted deficiency of KLF4 develop heart failure precipitously in response to pressure-overload but the underlying mechanisms remain unknown. We hypothesized that KLF4 may regulate mitochondrial function in the heart. Here we show that KLF4 governs mitochondrial biogenesis, metabolic function, dynamics and autophagic clearance. Adult mice with cardiac-specific KLF4 deficiency develop cardiac dysfunction with aging or in response to pressure overload characterized by reduced myocardial ATP levels, elevated ROS, and marked alterations in mitochondrial heterogeneity and alignment. Studies in mitochondria isolated from KLF4-deficient hearts revealed reduced respiration rate likely due to defects in ETC Complex I. Further, embryonic cardiac KLF4 deletion resulted in postnatal premature mortality, impaired mitochondrial biogenesis, and altered mitochondrial maturation. Mechanistically, we show that KLF4 binds to, cooperates with, and is requisite for optimal function of the ERR/PGC-1 transcriptional regulatory module on metabolic and mitochondrial targets. Finally, KLF4 also regulates autophagy through transcriptional control of a broad array of autophagy genes in cardiomyocytes. Collectively, these findings identify KLF4 as a nodal transcriptional regulator of mitochondrial homeostasis.

scholarly journals The Cardioprotective Signaling Activity of Activated Protein C in Heart Failure and Ischemic Heart Diseases

2019 ◽  
Vol 20 (7) ◽  
pp. 1762 ◽  
Author(s):  
Di Ren ◽  
Hemant Giri ◽  
Ji Li ◽  
Alireza R. Rezaie
Keyword(s):  
Heart Failure ◽  
Protein C ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Activated Protein C ◽  
Ischemic Heart ◽  
Signaling Networks ◽  
Endothelial Protein C Receptor ◽  
Signaling Mechanism ◽  
Mtorc1 Signaling

Activated protein C (APC) is a vitamin-K dependent plasma serine protease, which functions as a natural anticoagulant to downregulate thrombin generation in the clotting cascade. APC also modulates cellular homeostasis by exhibiting potent cytoprotective and anti-inflammatory signaling activities. The beneficial cytoprotective effects of APC have been extensively studied and confirmed in a number of preclinical disease and injury models including sepsis, type-1 diabetes and various ischemia/reperfusion diseases. It is now well-known that APC modulates downstream cell signaling networks and transcriptome profiles when it binds to the endothelial protein C receptor (EPCR) to activate protease-activated receptor 1 (PAR1) on various cell types. However, despite much progress, details of the downstream signaling mechanism of APC and its crosstalk with other signaling networks are far from being fully understood. In this review, we focus on the cardioprotective properties of APC in ischemic heart disease and heart failure with a special emphasis on recent discoveries related to the modulatory effect of APC on AMP-activated protein kinase (AMPK), PI3K/AKT, and mTORC1 signaling pathways. The cytoprotective properties of APC might provide a novel strategy for future therapies in cardiac diseases.

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