Cardiology Research最新文献

Our understanding of dilated cardiomyopathy (DCM) is evolving as new insights into the underlying pathophysiology become available. Professional organizations and clinical experts are improving definitions of DCM, allowing for more accurate treatment recommendations. This review summarized key published literature describing definitions and/or diagnostic criteria for DCM. Embase was searched from database inception to September 19, 2022 for 1) publications reporting definitions of DCM by major professional organizations and related opinion papers, and 2) clinical studies in DCM and heart failure with reduced ejection fraction. Sixty-eight records were included in this review. Definitions of DCM provided by two major professional organizations (American Heart Association (AHA) and European Society of Cardiology (ESC)) agreed on the clinical presentation of DCM; however, they differed in the classification of DCM within the larger context of cardiomyopathy taxonomies. Both organizations agreed that DCM could be clinically defined by the presence of left ventricular dilation and contractile dysfunction in the absence of abnormal loading conditions and severe coronary artery disease. AHA guidelines divided cardiomyopathies into two major groups (primary and secondary) based on predominant organ involvement. DCM was classified as primary cardiomyopathy with mixed (genetic and/or acquired) etiology. Conversely, ESC published a clinically oriented taxonomy in which cardiomyopathies were grouped into specific morphological and functional phenotypes; each was subclassified into familial or non-familial forms. Opinion papers further elaborated on the complex interplay between genetics and environment in the etiology of DCM. Several articles summarized the importance of the new and updated diagnostic tools, such as cardiac magnetic resonance imaging, electrocardiogram, and other biomarkers, in correctly identifying the etiology of DCM. Within clinical studies, most inclusion criteria used standard definitions proposed by leading professional associations (AHA and ESC). Clinical study investigators sometimes used a narrower definition of DCM using additional criteria for the left ventricular ejection fraction threshold value and left ventricular dilatation. Current efforts in cardiology research are focused on a more granular understanding of DCM etiology and the natural history of the disease. Definitions of DCM found in clinical studies mainly rely on published guidelines, with some studies adding idiosyncratic inclusion criteria refining the broad definitions of DCM.

Chronic coronary syndrome (CCS) is a long-term manifestation of coronary artery disease, marked by stable but recurring chest pain and myocardial ischemia due to the gradual buildup of atherosclerotic plaques in the coronary arteries. It is a metabolic disorder of coronary arteries characterized by oxidative stress, endothelial dysfunction, inflammation, and hyperlipidemia. The imbalance in oxidative-antioxidative status contributes to stable ischemic heart disease. Oxidative stress involves reactive oxygen and nitrogen species, leading to low-density lipoprotein (LDL) oxidation. Endothelial dysfunction, marked by reduced nitric oxide (NO) bioavailability, is an early onset of CCS, affecting vasodilation, cell proliferation, and inflammatory responses. Enzyme myeloperoxidase (MPO), traditionally considered protective, plays a dual role in initiating and progressing inflammatory diseases. MPO interacts with NO, modulating its catalytic activity. Elevated NO levels inhibit MPO through a reversible complex formation, preventing NO-induced inhibition by inducible nitric oxide synthase (iNOS). MPO also inactivates endothelial nitric oxide synthase (eNOS) and reacts with L-arginine, hindering NO synthesis. The interplay between MPO and NO significantly influences inflammation sites, impacting peroxidation rates and oxidation reactions. Peroxynitrite, a reactive species, contributes to nitration of tyrosine residues and lipid peroxidation. Mechanistic pathways suggest MPO enhances iNOS catalytic activity, influencing CCS development. iNOS, implicated in inflammation and atherosclerosis, is connected to NO regulation. This review analyzes the complex interplay of MPO, iNOS, and NO that affects plaque morphology, oxidative stress, and inflammation, contributing to atherosclerosis progression. Therefore, it is possible that the phenotypes of atherosclerotic plaques, focal and diffuse coronary artery disease, could be defined by the relationship between MPO and iNOS.

Background: In Indonesia, heart failure has become a major community problem because of the high cost of care, low quality of life, and premature death. Until now, loop diuretics are still the main therapy in patients with acute decompensated heart failure with clinical congestion. Diuretic responsiveness can be assessed objectively by measuring sodium urine. This study aimed to determine the response of natriuresis 2 h after loop diuretic administration and its relationship to length of stay and readmission within 30 days in daily clinical practice.

Methods: This is a prospective cohort study conducted at the National Cardiovascular Center Harapan Kita Hospital in acute decompensated heart failure patients. Patient characteristics were collected from medical records. Response to intravenous (IV) loop diuretics was assessed using urinary sodium laboratory panels. The primary outcomes of interest in this study were length of stay and rehospitalization. Analyses were conducted between the outcome of interests and patient characteristics.

Results: There were 51 acute decompensated heart failure patients in this study with 78.4% males. The mean age was 52.47 ± 13.62. The mean ejection fraction was 37.53±17.95%, with the majority of patients having a left ventricular ejection fraction less than 40% (62.7% of study subjects). The average glomerular filtration rate of subjects in this study was 57.29 ± 27.25 mL/min. Pearson correlation test between pre- and post-loop diuretic urinary sodium showed trends of significant correlation (r = -0.238, P = 0.093) and (r = -0.308, P = 0.028), respectively. Patients with lower pre-loop diuretic urinary sodium were shown to have a shorter length of stay (8.57 ± 6.161 vs. 5.30 ± 4.01, P = 0.04), while patients with lower post-loop diuretic urinary sodium showed trends of longer length of stay (8.67 ± 4.14 vs. 6.03 ± 5.39, P = 0.126).

Conclusions: In this study, we observe lower rehospitalization in patients with higher pre-loop diuretic urinary sodium levels. Post-loop diuretic urinary sodium level was shown to be inversely related to length of stay in acute decompensated heart failure patients.

Background: This study aimed to investigate if remote ischemic preconditioning reduces the inflammatory process on patients undergoing coronary artery bypass grafting (CABG).

Methods: We conducted a case-control study involving 80 patients, half of whom underwent ischemic preconditioning for severe coronary artery disease (CAD) and subsequently underwent CABG. We assessed interleukin (IL)-1 and IL-6 levels using the enzyme-linked immunosorbent assay (ELISA) method, high-sensitivity troponin I (hsTnI) using chemiluminescent immunoassay (CLIA), and C-reactive protein (CRP) using the turbidimetric method at three key time points: before surgery (visit 1 or V1), immediately postoperatively (visit 2 or V2), and 1 week postoperatively (visit 3 or V3) in all subjects.

Results: Ischemic preconditioned patients showed a significant decrease in proinflammatory markers (IL-1, IL-6) but not in CRP or hsTnI.

Conclusions: This study demonstrated that remote ischemic preconditioning significantly reduced the levels of specific proinflammatory markers (IL-1 and IL-6), which may suggest general systemic protection. However, it did not demonstrate cardioprotection per se, as evidenced by the absence of a statistically significant decrease in hsTnI level.

Chronic Chagas cardiomyopathy (CCC) poses significant health challenges not only in Latin America but also in non-endemic regions due to global migration. The complexity and severity of CCC call for an updated and thorough review to inform clinical practices and direct future research efforts. This review seeks to consolidate current knowledge on CCC, emphasizing diagnostic, therapeutic, and prognostic facets to facilitate better management and understanding of the disease. An exhaustive examination was conducted, analyzing peer-reviewed articles published between January 2020 and April 2024, sourced from prominent medical databases such as PubMed and Scopus. The review delineates crucial aspects of CCC pathophysiology, evaluates patient outcomes, identifies diagnostic challenges, and assesses treatment efficacy. Our findings prompt the need for revised clinical guidelines and stress the importance of continued research to enhance therapeutic strategies and disease comprehension. It is imperative that future studies address these identified gaps to advance patient care and treatment options for CCC.

Background: Hypertrophic cardiomyopathy (HCM) is one of the most prevalent inherited disorders and a common cause of sudden heart death. Left atrial (LA) dilatation frequently occurs in patients with HCM as a result of impaired left ventricular (LV) relaxation or associated involvement of LA myocardium in HCM.

Methods: We enrolled 170 patients known to had HCM (non-obstructive type) and 30 healthy subjects (control group). All of them underwent two-dimensional (2D) echocardiography to measure LV dimensions, function, LA dimension, LA deformations, pulmonary artery pressure (PAP) and LV global longitudinal strain (LVGLS). LA volumes and mechanics were also measured by three-dimensional (3D) echocardiography.

Results: By 2D echocardiography, patient group revealed significantly lower all LA functions vs. control group including reservoir (26 ± 4 vs. 43 ± 3, P < 0.001), conduit (-14 ± 2 vs. -25 ± 2, P < 0.001), and booster pump functions (-12 ± 2 vs. -18 ± 1, P < 0.001). PAP was significantly higher in patient group (42 ± 7 vs. 27 ± 4 in control group). LVGLS was significantly lower in patient group (-15±1.4% vs. -23±2% in control group). Using 3D speckle tracking echocardiography (STE), there were a significantly higher indexed maximum LA volume (Vmax indexed) (43.5 ± 5.6 vs. 28.7 ± 3.7, P < 0.001), but significantly lower left atrial strain at reservoir function (LASr) (24 ± 4 vs. 41 ± 3, P < 0.001), left atrial strain at conduit function (LAScd) (-13 ± 2 vs. -24 ± 2, P < 0.001), and left atrial strain at contractile function (LASct) (-11 ± 2 vs. -18 ± 1, P < 0.001).

Conclusion: Three-dimensional transthoracic echocardiography (TTE) is a feasible method for the assessment of LA remodeling, but there is adverse LA remodeling in patients with long-standing non-obstructive HCM including impaired all LA mechanics and with increased septal thickness, there are more diastolic dysfunction and more reduction of LA mechanics.

Background: The H₂FPEF score, a convenient tool developed for diagnosing heart failure with preserved ejection fraction (HFpEF), exhibited useful prognostic utility in HFpEF. However, the applicability and the prognostic value of the H₂FPEF score in Chinese HFpEF patients have yet to be fully confirmed. The study aimed to evaluate the effect of modified H₂FPEF score on the prognosis of Chinese HFpEF patients.

Methods: In this retrospective study, we calculated the H₂FPEF scores by body mass index (BMI) ≥ 25 kg/m² and 30 kg/m² respectively, for 497 consecutive HFpEF patients in China. Subjects were divided into low- (0 - 3 points), intermediate- (4 - 6 points), and high-score (7 - 9 points) groups. The primary and secondary endpoints were heart failure (HF)-related events and acute coronary syndrome (ACS), respectively. Cox proportional hazard models were applied to calculate hazard ratios (HRs). Receiver operating characteristic (ROC) curves and areas under the curve (AUC) were used to evaluate the prediction of the H₂FPEF score for adverse outcomes.

Results: Over a mean follow-up of 40.46 ± 6.52 months, the primary and secondary endpoints occurred in 168 patients (33.8%) and 97 patients (19.5%), respectively. By the definition of obesity as BMI ≥ 25 kg/m², a higher incidence of HF-related events and ACS was observed among those with a higher modified H₂FPEF score. The modified H₂FPEF significantly predicted HF-related events (AUC: 0.723; 95% confidence interval (CI): 0.676 - 0.770; P < 0.001) and ACS (AUC: 0.670; 95% CI: 0.608 - 0.731; P < 0.014) with higher power than the H₂FPEF score calculated by BMI ≥ 30 kg/m². The cutoff of the modified H₂FPEF score was 6.5 for detecting HF-related events and ACS.

Conclusions: The modified H₂FPEF score, using BMI ≥ 25 kg/m² to define obesity, could more effectively predict the occurrence of subsequent cardiovascular events in Chinese HFpEF patients. The modified H₂FPEF score above 6.5 is a risk factor for adverse cardiovascular events in HFpEF patients.

Background: Previous investigations have established the anti-inflammatory properties of fibroblast growth factor 21 (FGF21). However, the specific mechanism through which FGF21 mitigates myocardial ischemia/reperfusion (I/R) injury by inhibiting neutrophil extracellular traps (NETs) remains unclear.

Methods: A mice model of myocardial I/R injury was induced, and myocardial tissue was stained with immunofluorescence to assess NETs. Serum NETs levels were quantified using a PicoGreen kit. In addition, the expression levels of adenosine monophosphate (AMP)-activated protein kinase (AMPK) and FGF21 were evaluated by Wes fully automated protein blotting quantitative analysis system. Moreover, a hypoxia/reoxygenation (H/R) model was established using AMPK inhibitor and agonist pretreated H9c2 cells to further explore the relationship between FGF21 and AMPK.

Results: Compared with the control group, serum NETs levels were significantly higher in I/R mice, and a large number of NETs were formed in myocardial tissues (97.63 ± 11.45 vs. 69.65 ± 3.33, P < 0.05). However, NETs levels were reversed in FGF21 pretreated mice (P < 0.05). Further studies showed that FGF21 enhanced AMPK expression, which was significantly increased after inhibition of AMPK and decreased after promotion of AMPK (P < 0.05).

Conclusions: FGF21 may exert cardioprotective effects by inhibiting I/R injury-induced NETs via AMPK.

Background: Left ventricular noncompaction (LVNC) is recognized within the spectrum of adult cardiomyopathies for its unique pathophysiologic features and clinical challenges. This condition exhibits a wide range of clinical manifestations, from asymptomatic states to severe cardiovascular complications, making its diagnosis and management challenging. This study aimed to synthesize current data on the prevalence, diagnostic methods, clinical outcomes, and treatment efficacy of LVNC in adults to address gaps in understanding and management strategies.

Methods: A systematic review and meta-analysis of research from 2000 to March 2024 was conducted, focusing on studies involving adults diagnosed with LVNC. This approach aimed to collect data on the prevalence of LVNC, the diagnostic accuracy of different imaging modalities, clinical manifestations, and the impact of different treatment strategies.

Results: The study showed a prevalence of LVNC of 0.5%, with cardiovascular magnetic resonance outperforming echocardiography in diagnosis with a detection rate of 1.3%. Mortality and heart transplantation rates were 12% and 7%, respectively. Significant predictors of adverse outcomes included New York Heart Association (NYHA) class III or IV, ventricular tachycardia, and reduced left ventricular ejection fraction (LVEF), guiding a nuanced approach in tailoring therapeutic strategies to optimize patient care and outcomes.

Conclusions: This study advances the understanding of LVNC by refining diagnostic criteria and evaluating management strategies, highlighting the superiority of cardiovascular magnetic resonance. It identifies predictors of adverse outcomes and assesses treatment efficacy, urging precision in diagnosis and tailored treatments. Its comprehensive analysis and methodological rigor make it a key resource advocating a multidisciplinary approach to improve patient outcomes in LVNC.

A 63-year-old female presented to a freestanding emergency room with dizziness, palpitations, and hypotension, The patient was found to have an irregular wide complex tachycardia, consistent with ventricular tachycardia, hypomagnesemia and severe hypocalcemia. The tachycardia was refractory to treatment with IV amiodarone and magnesium, and only resolved with correction of the serum calcium. Review of the medical record revealed an echocardiogram 19 years earlier reporting left ventricular dysfunction. The patient was unaware of this diagnosis and was not taking medical therapy. Echocardiogram revealed no significant change in left ventricular function, and coronary angiography showed no significant coronary artery disease. The patient's nonischemic cardiomyopathy may have been a predisposing factor for the arrhythmia presentation. We explore a hospital admission involving the rare association of hypocalcemia and monomorphic ventricular tachycardia, which is not well documented in the literature.