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The American Journal of Cardiology Feb 2024Hypertrophic cardiomyopathy (HCM) is a complex, heterogeneous disorder that affects approximately 1 in every 500 persons worldwide and about 750,000 Americans. It is... (Review)
Review
Hypertrophic cardiomyopathy (HCM) is a complex, heterogeneous disorder that affects approximately 1 in every 500 persons worldwide and about 750,000 Americans. It is characterized by left ventricular hypertrophy that is usually asymmetric, with enlarged myocytes in disarray, unexplained by loading conditions. Obstruction to left ventricular outflow occurs in approximately 60% of patients. The natural history and cardiac morphology of HCM are quite heterogeneous. Although most patients with HCM are asymptomatic or mildly symptomatic, a minority are disabled by dyspnea, angina, or syncope, develop advanced heart failure, or die suddenly.
Topics: Humans; Cardiomyopathy, Hypertrophic; Death, Sudden, Cardiac; Heart Failure; Heart Ventricles; Hypertrophy, Left Ventricular; Syncope
PubMed: 38368032
DOI: 10.1016/j.amjcard.2023.10.075 -
Hypertension Research : Official... Mar 2024
Topics: Humans; Blood Pressure; Hypertrophy, Left Ventricular; Blood Glucose; Japan; Hypertension; Diabetes Mellitus
PubMed: 38148349
DOI: 10.1038/s41440-023-01562-x -
The Journal of Heart and Lung... Feb 2024Right ventricular failure (RVF) is a leading cause of morbidity and mortality in multiple cardiovascular diseases, but there are no treatments for RVF as therapeutic...
BACKGROUND
Right ventricular failure (RVF) is a leading cause of morbidity and mortality in multiple cardiovascular diseases, but there are no treatments for RVF as therapeutic targets are not clearly defined. Contemporary transcriptomic/proteomic evaluations of RVF are predominately conducted in small animal studies, and data from large animal models are sparse. Moreover, a comparison of the molecular mediators of RVF across species is lacking.
METHODS
Transcriptomics and proteomics analyses defined the pathways associated with cardiac magnetic resonance imaging (MRI)-derived values of RV hypertrophy, dilation, and dysfunction in control and pulmonary artery banded (PAB) pigs. Publicly available data from rat monocrotaline-induced RVF and pulmonary arterial hypertension patients with preserved or impaired RV function were used to compare molecular responses across species.
RESULTS
PAB pigs displayed significant right ventricle/ventricular (RV) hypertrophy, dilation, and dysfunction as quantified by cardiac magnetic resonance imaging. Transcriptomic and proteomic analyses identified pathways associated with RV dysfunction and remodeling in PAB pigs. Surprisingly, disruptions in fatty acid oxidation (FAO) and electron transport chain (ETC) proteins were different across the 3 species. FAO and ETC proteins and transcripts were mostly downregulated in rats but were predominately upregulated in PAB pigs, which more closely matched the human response. All species exhibited similar dysregulation of the dilated cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy pathways.
CONCLUSIONS
The porcine metabolic molecular signature was more similar to human RVF than rodents. These data suggest there may be divergent molecular responses of RVF across species, and pigs may more accurately recapitulate metabolic aspects of human RVF.
Topics: Humans; Rats; Animals; Swine; Ventricular Dysfunction, Right; Multiomics; Proteomics; Heart Failure; Hypertrophy, Right Ventricular; Ventricular Function, Right; Disease Models, Animal; Ventricular Remodeling
PubMed: 37783299
DOI: 10.1016/j.healun.2023.09.020 -
European Journal of Radiology Dec 2023Regardless of whether there are morphological abnormalities of right ventricle in hypertrophic cardiomyopathy (HCM) patients, the exact contribution of right ventricular...
PURPOSE
Regardless of whether there are morphological abnormalities of right ventricle in hypertrophic cardiomyopathy (HCM) patients, the exact contribution of right ventricular (RV) global strains remains unresolved. We aimed to study the prognostic value of RV global strains in HCM patients with and without RV hypertrophy (RVH).
METHOD
A total of 358 HCM patients who underwent the CMR examination and carried out the follow-up were finally included in this retrospective study. The endpoint was a composite of all-cause mortality, aborted SCD, and heart failure readmission. RV hypertrophy (RVH) was defined as maximal RVWT ≥ 5 mm at end-diastole. RV global strains (RV global longitudinal strain (GLS) and RV global circumferential strain (GCS) were measured in HCM patients by cardiac MRI feature tracking technique. The intraobserver and interobserver reproducibility were evaluated. Receiver-operating characteristic curves and Kaplan-Meier curves, cox proportional hazards regression, Likelihood ratio test and Integrated Discrimination Improvement (IDI) analysis were performed. P-value were corrected for multiple testing when using many covariables by a false discovery rate adjustment.
RESULTS
Over a median follow-up of 25 (range 3-54) months, 49 patients reached the composite endpoints. HCM patients were divided into the RVH group and non-RVH groups. In the multivariate cox proportional hazards regression, after adjusting multiple clinical and imaging variables, RV GLS and RV GCS were independently associated with the composite endpoints in the RVH group (HR: 1.123; 95 % CI: 1.048-1.205; P = 0.002) and non-RVH group (HR: 1.174; 95 % CI: 1.031-1.337; P = 0.015), respectively. And The IDI index of models improved when adding RV GLS (IDI = 0.030, p < 0.001) and RV GLS (IDI = 0.056, p = 0.020), respectively.
CONCLUSIONS
RV GLS and RV GCS are independent predictors of HCM with RVH and without RVH, respectively. RV GLS in the RVH group and RV GCS in the non-RVH group provide additional values for predicting the risk of adverse events.
Topics: Humans; Hypertrophy, Right Ventricular; Retrospective Studies; Heart Ventricles; Reproducibility of Results; Cardiomyopathy, Hypertrophic; Prognosis; Stroke Volume
PubMed: 37871355
DOI: 10.1016/j.ejrad.2023.111148 -
Journal of the American Heart... Feb 2024Alveolar hypoxia is protective in the context of cardiovascular and ischemic heart disease; however, the underlying mechanisms are incompletely understood. The present...
BACKGROUND
Alveolar hypoxia is protective in the context of cardiovascular and ischemic heart disease; however, the underlying mechanisms are incompletely understood. The present study sought to test the hypothesis that hypoxia is cardioprotective in left ventricular pressure overload (LVPO)-induced heart failure. We furthermore aimed to test that overlapping mechanisms promote cardiac recovery in heart failure patients following left ventricular assist device-mediated mechanical unloading and circulatory support.
METHODS AND RESULTS
We established a novel murine model of combined chronic alveolar hypoxia and LVPO following transverse aortic constriction (HxTAC). The HxTAC model is resistant to cardiac hypertrophy and the development of heart failure. The cardioprotective mechanisms identified in our HxTAC model include increased activation of HIF (hypoxia-inducible factor)-1α-mediated angiogenesis, attenuated induction of genes associated with pathological remodeling, and preserved metabolic gene expression as identified by RNA sequencing. Furthermore, LVPO decreased and increased mRNA expression under normoxic conditions, which was attenuated under hypoxic conditions and may induce additional hypoxia-mediated cardioprotective effects. Analysis of samples from patients with advanced heart failure that demonstrated left ventricular assist device-mediated myocardial recovery revealed a similar expression pattern for and as observed in HxTAC hearts.
CONCLUSIONS
Hypoxia attenuates LVPO-induced heart failure. Cardioprotective pathways identified in the HxTAC model might also contribute to cardiac recovery following left ventricular assist device support. These data highlight the potential of our novel HxTAC model to identify hypoxia-mediated cardioprotective mechanisms and therapeutic targets that attenuate LVPO-induced heart failure and mediate cardiac recovery following mechanical circulatory support.
Topics: Humans; Mice; Animals; Heart Failure; Cardiomegaly; Myocardium; Aortic Valve Stenosis; Hypoxia; Ventricular Remodeling; Disease Models, Animal
PubMed: 38293923
DOI: 10.1161/JAHA.123.033553 -
Arquivos Brasileiros de Cardiologia 2023Weight gain can trigger mechanisms that increase blood pressure. Nevertheless, obesity causes structural changes in the myocardium, including increased ventricular mass,...
BACKGROUND
Weight gain can trigger mechanisms that increase blood pressure. Nevertheless, obesity causes structural changes in the myocardium, including increased ventricular mass, atrial dilatation, and diastolic and systolic dysfunction. Additionally, blood pressure variations, like morning surge (MS) in obese hypertensive patients may have clinical relevance in cardiovascular events. Although morning blood pressure surge is a physiological phenomenon, excess MS can be considered an independent risk factor for cardiovascular events.
OBJECTIVE
To evaluate MS values and their association with left ventricular hypertrophy (LVH) and nocturnal dipping (ND) in obese and non-obese hypertensive patients.
METHODS
A cross-sectional study that evaluated BP measurements by ambulatory blood pressure monitoring (ABPM) and the presence of LVH by echocardiography in 203 hypertensive outpatients, divided into two groups: 109 non-obese and 94 obese hypertensives patients. The significance level was set at 0.05 in two-tailed tests.
RESULTS
A MS above 20 mmHg by ABPM was detected in 59.2% of patients in the non-obese group and 40.6% in the obese group. LVH was found in 18.1% and 39.3% of patients in the non-obese and obese groups, respectively, p<0.001. In the "obese group", it was observed that a MS>16 mmHg was associated with LVH, [prevalence ratio: 2.80; 95%CI (1.12-6.98), p=0.03]. For the non-obese group, the cut-off point of MS for this association was >22 mmHg.
CONCLUSION
High MS was positively associated with LVH, with a particular behavior in the hypertensive obese group.
Topics: Humans; Blood Pressure Monitoring, Ambulatory; Hypertrophy, Left Ventricular; Cross-Sectional Studies; Hypertension; Blood Pressure; Obesity
PubMed: 37820172
DOI: 10.36660/abc.20230050 -
Current Opinion in Cardiology Jul 2024Left ventricular (LV) hypertrophy (LVH) is a well recognized target organ adaptation to longstanding uncontrolled hypertension and other cardiovascular risk factors. It... (Review)
Review
PURPOSE OF REVIEW
Left ventricular (LV) hypertrophy (LVH) is a well recognized target organ adaptation to longstanding uncontrolled hypertension and other cardiovascular risk factors. It is also a strong and independent predictor of many cardiovascular disorders.
RECENT FINDINGS
This focused review explores the current concepts in screening, diagnosis, prevention, and treatment of LVH in patients with hypertension. Currently, the primary screening and diagnostic tools for LVH are ECG and 2D echocardiography. Implementing machine learning in the diagnostic modalities can improve sensitivity in the detection of LVH. Lifestyle modifications, blood pressure control with antihypertensive therapy, and management of comorbidities aid in preventing and reversing LV remodeling.
SUMMARY
LVH is a common and often silent complication of hypertension. Prevention and reversal of LV remodeling are crucial for cardiovascular risk reduction in patients with hypertension.
Topics: Humans; Hypertrophy, Left Ventricular; Hypertension; Antihypertensive Agents; Ventricular Remodeling; Echocardiography
PubMed: 38603529
DOI: 10.1097/HCO.0000000000001135 -
Hypertension (Dallas, Tex. : 1979) Sep 2023
Topics: Humans; Blood Pressure; Hypertrophy, Left Ventricular; Hypertension; Antihypertensive Agents; Heart
PubMed: 37585540
DOI: 10.1161/HYPERTENSIONAHA.123.21512 -
Journal of Electrocardiology 2023The U-wave's electrophysiological origin remains unknown and is subject to debate. It is rarely used for diagnosis in clinical practice. The aim of this study was to... (Review)
Review
UNLABELLED
The U-wave's electrophysiological origin remains unknown and is subject to debate. It is rarely used for diagnosis in clinical practice. The aim of this study was to review new information regarding the U-wave. Further to present the proposed theories behind the U-wave's origin along with potential pathophysiologic and prognostic implications related to its presence, polarity and morphology.
METHOD
Literature searches were conducted to retrieve publications related to the electrocardiogram U-wave in the literature database Embase.
RESULTS
The review of the literature revealed the following major theories that will be discussed; late depolarisation, delayed or prolonged repolarisation, electro-mechanical stretch and IK1 dependent intrinsic potential differences in the terminal part of the action potential. Various pathologic conditions were found to correlate with the presence and properties of the U-wave, such as its amplitude and polarity. Abnormal U-waves can, for example, be observed in coronary artery disease with ongoing myocardial ischemia or infarction, ventricular hypertrophy, congenital heart disease, primary cardiomyopathy and valvular defects. Negative U-waves are highly specific for the presence of heart diseases. Concordantly negative T- and U-waves are especially associated with cardiac disease. Patients with negative U-waves tend to have higher blood pressure and history of hypertension, higher heart rate, cardiac disease and left ventricular hypertrophy compared to subjects with normal U-waves. Negative U-waves have been found to be associated with increased risk of all-cause mortality, cardiac death and cardiac hospitalisation in men.
CONCLUSIONS
The origin of the U-wave is still not established. U-wave diagnostics may reveal cardiac disorders and the cardiovascular prognosis. Including the U-wave characteristics in the clinical ECG assessment may be useful.
Topics: Male; Humans; Electrocardiography; Heart; Myocardial Ischemia; Hypertrophy, Left Ventricular; Hypertension; Heart Defects, Congenital; Coronary Artery Disease
PubMed: 36907158
DOI: 10.1016/j.jelectrocard.2023.03.001 -
Life Sciences Sep 2023Heart failure typically occurs early in the clinical course of sustained cardiac hypertrophy that is accompanied by maladaptive remodeling of the heart. It is critical...
Heart failure typically occurs early in the clinical course of sustained cardiac hypertrophy that is accompanied by maladaptive remodeling of the heart. It is critical to discover new mechanisms and effective therapeutic targets to prevent and cure pathological cardiac hypertrophy. The objective of the study was to evaluate the effects of circRNAs on NSD2-induced ventricular remodeling. We screened the dysregulated circRNAs in normal or NSD2 C57BL/6 mice with or without transverse aortic constriction (TAC), and found that circCmss1 significantly increased in normal TAC mice, but decreased in NSD2 TAC mice. Angiotensin II(Ang II)induced neonatal cardiomyocyte hypertrophy in vitro and the pressure overload-induced cardiac hypertrophy in vivo can be reduced by Knocking down circCmss1. We further investigated the downstream signaling of circCmss1 in the progression of NSD2-promoted ventricular remodeling and discovered that circCmss1 could interact with a transcription factor EIF4A3 and induce the expression of transferrin receptor 1 (TfR1), thus activating the ferroptosis in cardiomyocytes. This study highlights the significance of NSD2 activation of circCmss1/EIF4A3/TfR1 as therapeutic targets for treating pathological myocardial hypertrophy.
Topics: Animals; Mice; Cardiomegaly; Ferroptosis; Mice, Inbred C57BL; Myocytes, Cardiac; RNA, Circular; Ventricular Remodeling
PubMed: 37352916
DOI: 10.1016/j.lfs.2023.121873