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Ventricular tachycardia (VT) is an arrhythmia that originates from the ventricles of the heart and presents as a wide and prolonged QRS complex on the electrocardiograph of greater than 120 milliseconds, with a heart rate of over 100 beats per minute. VT can occur as a pulsed or pulseless rhythm. Pulseless VT occurs when the ventricles cannot effectively pump blood out of the heart, therefore resulting in no cardiac output. Pulsed VT can manifest with the patient presenting asymptomatically, or with symptoms of reduced cardiac output resulting from poor ventricular filling. There is the potential for the patient to quickly become haemodynamically unstable if not treated. This article discusses a case of pulsed VT, diagnosed and treated out of hours in an acute hospital. [ABSTRACT FROM AUTHOR]

Heat shock protein 27 (HSP27) is a small chaperone protein that is overexpressed in a variety of cellular stress states. It is involved in regulating proteostasis and protecting cells from multiple sources of stress injury by stabilizing protein conformation and promoting the refolding of misfolded proteins. Previous studies have confirmed that HSP27 is involved in the development of cardiovascular diseases and plays an important regulatory role in this process. Herein, we comprehensively and systematically summarize the involvement of HSP27 and its phosphorylated form in pathophysiological processes, including oxidative stress, inflammatory responses, and apoptosis, and further explore the potential mechanisms and possible roles of HSP27 in the diagnosis and treatment of cardiovascular diseases. Targeting HSP27 is a promising future strategy for the treatment of cardiovascular diseases.

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. Recent studies have shown that n6-methyladenosine (m6A) plays a major role in cardiovascular homeostasis and pathophysiology. These studies have confirmed that m6A methylation affects the pathophysiology of cardiovascular diseases by regulating cellular processes such as differentiation, proliferation, inflammation, autophagy, and apoptosis. Moreover, plenty of research has confirmed that m6A modification can delay the progression of CVD via the post-transcriptional regulation of RNA. However, there are few available summaries of m6A modification regarding CVD. In this review, we highlight advances in CVD-specific research concerning m6A modification, summarize the mechanisms underlying the involvement of m6A modification during the development of CVD, and discuss the potential of m6A modification as a therapeutic target of CVD. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. Recent studies have shown that n6-methyladenosine (m6A) plays a major role in cardiovascular homeostasis and pathophysiology. These studies have confirmed that m6A methylation affects the pathophysiology of cardiovascular diseases by regulating cellular processes such as differentiation, proliferation, inflammation, autophagy, and apoptosis. Moreover, plenty of research has confirmed that m6A modification can delay the progression of CVD via the post-transcriptional regulation of RNA. However, there are few available summaries of m6A modification regarding CVD. In this review, we highlight advances in CVD-specific research concerning m6A modification, summarize the mechanisms underlying the involvement of m6A modification during the development of CVD, and discuss the potential of m6A modification as a therapeutic target of CVD.

New-onset atrial fibrillation (NOAF), both early (EAF) or late (LAF), may complicate ST-segment elevation myocardial infarction (STEMI). The mechanisms underlying EAF or LAF are poorly described. We investigated atrial branch occlusion and EAF or LAF onset in STEMI patients undergoing primary percutaneous coronary intervention. This was a retrospective cohort study including 155 STEMI patients. Patients were divided into 3 groups: sinus rhythm (SR), EAF, or LAF. Clinical characteristics, angiographic features including occlusion of atrial branches, namely ramus ostia cavae superioris (ROCS), atrio-ventricular node artery (AVNA), right intermediate atrial artery (RIAA), and left intermediate atrial artery, were assessed. We also investigated in-hospital adverse events (AEs) and death. Mean age was 63.8±11.9 years; 78.7% were men. NOAF was detected in 22 (14.2%) patients: 10 (6.4%) EAF and 12 LAF (7.7%). Compared to EAF, LAF patients were older (p =0.013), with higher GRACE risk score (p =0.014) and Killip class (p =0.015), depressed ejection fraction (p =0.007), elevated filling pressures (p =0.029), higher C-reactive protein (p =0.014) and more with thrombolysis in myocardial infarction flow <3 (p =0.015). Compared to SR, EAF was associated with higher prevalence of occluded ROCS (p =0.010), AVNA (p =0.005), and RIAA (p <0.001). Moreover, EAF patients had more frequently ≥2 diseased atrial branches than SR (19.5%, p <0.001) and LAF (25%, p <0.030) patients. LAF patients had a higher in-hospital AEs (p =0.019 vs SR; p =0.029 vs EAF) and death (p =0.004 vs SR). The occlusion of atrial branches is associated with EAF but not LAF following STEMI. LAF patients had worse in-hospital AEs and mortality. • Early and late atrial fibrillation (AF) after ST-segment elevated myocardial infarction have recently been described. • Whether atrial ischemia is associated with early or late AF is unknown. • Atrial branch occlusion is higher in patients with early but not late AF episodes. • Early AF episodes are associated with better in-hospital outcomes and mortality. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract Background Matrix metalloproteinase-9 (MMP-9) participates in the degradation of components of the extracellular matrix and it is involved in vascular remodeling and vasomotor changes. The aim of this study was to investigate the plasma levels of MMP-9 in acute vascular alterations due to hypertensive crisis. Methods This cross-sectional study was performed in 40 normotensive (NT) and 58 controlled hypertensive subjects (CHyp) followed up in outpatient clinic. Moreover, 57 patients with hypertensive emergency (HypEmerg) and 43 in hypertensive urgency (HypUrg), seen in emergency department, were also included. Hypertensive crisis was divided into HypEmerg, which was characterized by levels of systolic blood pressure (BP) ≥ 180 mmHg and/or diastolic BP ≥ 120 mmHg complicated with target-organ damage (TOD), and HypUrg, defined by BP elevation without TOD. Univariate and multivariate regression analysis was performed to identify the influence of independent variables on MMP-9 levels. A p-value

Lower BiVentricular (BiV) pacing percentages have been associated with significantly worse survival in patients with chronic heart failure (HF). However, the pathophysiology behind this observation has not been further delineated. This analysis evaluated whether small incremental decreases in BiV pacing percentages were associated with worse measures, related to HF physiology using individual sensor trends and the HeartLogic composite index. Sensor data was obtained from 900 ambulatory HF patients with implanted CRT devices. The percent of cardiac cycles with BiV pacing was assessed for periods (median = 7.3 days) between data downloads (median = 55 periods/patient). The third heart sound (S3), respiration rate, RSBI, and night-time heart rate were significantly elevated with sub-optimal pacing (<98%), while the first heart sound (S1), thoracic impedance, and activity were significantly lower. All sensor changes were in the direction associated with worsening HF. While IN the HeartLogic alert state (threshold above an Index of 16) the odds of optimal BiV pacing (≥98%) were less than when OUT of the HeartLogic alert state for a given subject (OR: 0.655; 95% CI: 0.626–0.686; p < 0.0001). The percent BiV pacing was reduced and the HeartLogic Index was increased in the periods surrounding HFhospitalizations. Lower BiV pacing percent is associated with multiple sensor changes indicative of worsening HF, and patients in HeartLogic alert are more likely to have suboptimal BiV pacing. Collectively, these data provide strong evidence that even small decreases in BiV percent pacing can lead to worsening HF. • Deteriorating sensor trends, associated heart failure worsening, were found with small decrements in BiV percent pacing. • Patients in HeartLogic alert are more likely to have suboptimal BiV pacing. • The percent BiV pacing was reduced, and the HeartLogic index was increased, preceding heart failure hospitalizations. • These observations support the recommendation to maximize BiV percent pacing, to improve the heart failure condition. [ABSTRACT FROM AUTHOR]

Background It is well known that after menopause women are exposed to a greater cardiovascular risk, but the intracellular modifications are not properly described. The sodium/proton exchanger (NHE) and the sodium/bicarbonate cotransporter (NBC) regulate the intracellular pH and, indirectly, the intracellular sodium concentration ([Na+]). There are 2 isoforms of NBC in the heart: the electrogenic (1Na+/2[Graphic: see text]; NBCe1) and the electroneutral (1Na+/1[Graphic: see text]; NBCn1). Because NHE and NBCn1 hyperactivity as well as the NBCe1 decreased activity have been associated with several cardiovascular pathologies, the aim of this study was to investigate the potential alterations of the alkalinizing transporters during the postmenopausal period. Methods and Results Three‐month ovariectomized rats (OVX) were used. The NHE activity and protein expression are significantly increased in OVX. The NBCe1 activity is diminished, and the NBCn1 activity becomes predominant in OVX rats. p‐Akt levels showed a significant diminution in OVX. Finally, NHE activity in platelets from OVX rats is also higher in comparison to sham rats, resulting in a potential biomarker of cardiovascular diseases. Conclusions Our results demonstrated for the first time that in the cardiac ventricular myocytes of OVX rats NHE and NBC isoforms are altered, probably because of the decreased level of p‐Akt, compromising the ionic intracellular homeostasis.

Background: Matrix metalloproteinase-9 (MMP-9) participates in the degradation of components of the extracellular matrix and it is involved in vascular remodeling and vasomotor changes. The aim of this study was to investigate the plasma levels of MMP-9 in acute vascular alterations due to hypertensive crisis.Methods: This cross-sectional study was performed in 40 normotensive (NT) and 58 controlled hypertensive subjects (CHyp) followed up in outpatient clinic. Moreover, 57 patients with hypertensive emergency (HypEmerg) and 43 in hypertensive urgency (HypUrg), seen in emergency department, were also included. Hypertensive crisis was divided into HypEmerg, which was characterized by levels of systolic blood pressure (BP) ≥ 180 mmHg and/or diastolic BP ≥ 120 mmHg complicated with target-organ damage (TOD), and HypUrg, defined by BP elevation without TOD. Univariate and multivariate regression analysis was performed to identify the influence of independent variables on MMP-9 levels. A p-value < 0.05 was considered statistically significant.Results: The mean age was 43.5 years in the NT group (11 men); 57.7 years in the CHyp group (29 men); 59.4 years in the HypUrg group (21 men) and 62.4 years in the HypEmerg group (31 men). The age was statistically different in the NT group compared to other 3 groups. The mean BP was 116.5 ± 13.9/72.4 ± 10.6 mmHg for NT, 123.2 ± 12.6/79 ± 9.2 for CHyp, 194.1 ± 24.3/121.4 ± 17.3 for HypUrg and 191.6 ± 34.3/121.7 ± 18.8 mmHg for HypEmerg, respectively (p-value< 0.0001 between groups). MMP-9 levels were statistically different between the HypEmerg (2.31 ± 0.2 ng/mL) and HypUrg groups (2.17 ± 0.3 ng/mL) compared to the NT (1.94 ± 0.3 ng/mL) (p-value < 0.01 and p-value < 0.05, respectively) and CHyp groups (1.92 ± 0.2 ng/mL) (p-value < 0.01). Uric acid was the only independent variable for predicting MMP-9 levels (p-value = 0.001).Conclusion: MMP-9 concentrations are significantly higher in the hypertensive crisis groups (urgency and emergency) compared to the control groups. Therefore, MMP-9 may be a biomarker or mediator of pathophysiologic pathways in cases of acute elevations of blood pressure. [ABSTRACT FROM AUTHOR]

Background: Sacrococcygeal teratomas (SCT) are often highly vascularized and may result in high-output cardiac failure, polyhydramnios, fetal hydrops, and demise. Delivery is guided by the SCT to fetus volume ratio (SCTratio), SCT growth rate, and cardiac output indexed for weight (CCOi).Methods: We compared measurements and outcome in 12 consecutive fetuses referred with SCT. Adverse outcomes were: fetal surgery, delivery < 32 gestational weeks or neonatal demise. Only SCTratio and CCOi were used to manage the cases. SCT vascularization index (VI%) was derived from the 3D virtual organ computer-aided analysis (VOCAL) software. The SCTModel (modified from acardiac twins) calculated a hypothetical SCT draining vein size and derived a risk line, using diameters of the superior and inferior vena cava, the azygous and umbilical veins. VI% and a model of systemic and umbilical venous volumes (SCTModel) were tested as indicators for outcome in SCT.Results: Fetuses were monitored from 20.1 to 36.4 gestational weeks and 5/12 had adverse outcomes: 1 had successful open fetal surgery at 23.8 weeks and delivered at term, 4 delivered at < 32 weeks with 3/4 having neonatal demise between 25 and 29 weeks. VI% was significantly higher in cases with adverse outcomes (mean 10.3 [8.9-11.6] vs. 4.4 [3.4-5.3], p < 0.0001). The additional fraction of the fetal cardiac output required to perfuse the SCT-draining vein (XSCO%) (p = 0.46), SCTratio (p = 0.08), and CCOi (p = 0.64) were not significant. All cases with adverse outcome had VI% > 8%. The SCTModel risk line predicted nonadverse outcomes well but lacked data in 2/5 cases with adverse outcomes.Conclusions: VI% is a significant indicator of SCT cases with adverse outcomes and combined with SCTratio may guide timing of delivery better than current measures. [ABSTRACT FROM AUTHOR]

The relationship between insulin resistance and coronary artery disease (CAD) is a crucial study area in understanding the complex connection between metabolic dysregulation and cardiovascular morbidity. This scholarly investigation examines the intricate relationship between insulin resistance, a key characteristic of metabolic syndrome, and CAD development. The goal is to understand the detailed molecular and physiological connections that underlie the dangerous connection between the endocrine and cardiac systems. The recognition of insulin resistance as a key player in cardiovascular disease highlights the need to study the complex relationships between insulin signaling pathways and the development of atherosclerosis. This research analyzes the molecular processes by which insulin resistance leads to disruptions in lipid metabolism, inflammatory reactions, and malfunction of the blood vessel's inner lining. These processes create an environment that promotes the development and advancement of CAD. As we begin this scientific exploration, it becomes clear that insulin resistance acts as a metabolic indicator and a potent mediator of endothelial dysfunction, oxidative stress, and systemic inflammation. The complex interaction between insulin-sensitive tissues and the vascular endothelium plays a crucial role in defining the pathophysiological landscape of CAD. Furthermore, this discussion highlights the mutual interaction between the endocrine and cardiac systems, where CAD produced by myocardial ischemia worsens insulin resistance through complex molecular pathways. Discovering new therapeutic targets that disrupt the harmful cycle between insulin resistance and the development of CAD shows potential for creating specific therapies to reduce cardiovascular risk in people with insulin resistance. This study aims to clarify the complexities of the connection between the endocrine system and the heart, establishing the basis for a thorough comprehension of how insulin resistance contributes to the development and advancement of CAD., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Ashraf et al.)

BACKGROUND Prehypertension (blood pressure (BP) of 120-139 mm Hg systolic and/ or 80-89 mm Hg diastolic) is highly prevalent and is associated with increased cardiovascular risk. Our goal was to investigate the extent to which prehypertension is associated with end-organ alterations in cardiac structure and function in a large biracial cohort of older men and women. METHODS We studied 4,871 participants of the Atherosclerosis Risk in Communities (ARIC) study who attended visit 5 (2011-2013) and underwent twodimensional echocardiography while free of prevalent coronary heart disease or heart failure. We categorized participants into 3 groups: optimal BP (BP <120 mm Hg and <80 mm Hg) (n = 402), prehypertension (n = 537), and hypertension (n = 3,932). RESULTS Individuals with prehypertension (75 ± 5 years) had higher left ventricular (LV) mass index and wall thickness, and higher prevalence of abnormal LV geometry than those with optimal BP (74 ± 5 years), but lower than those with frank hypertension (76 ± 5 years). In addition, participants with prehypertension had impairment of diastolic parameters (E/A, E' and E/E'), and had higher prevalence of mild and moderatesevere diastolic dysfunction compared to those with optimal BP, but no differences in systolic parameters. These differences in cardiac structure and function remained significant after adjusting for important clinical covariates. CONCLUSION In the ARIC cohort at visit 5, prehypertension was associated with increased LV remodeling and impaired diastolic function, but not systolic function, suggesting that even mildly elevated BP within the normal range is associated with cardiac end-organ damage. [ABSTRACT FROM AUTHOR]

The article focuses on the protection extended by diet-induced obesity against vascular defects in salt-sensitive rats. The study by the authors compared the middle cerebral arteries of salt-sensitive rats and SS.13BN consomic rats that were fed high-fat diet and normal-fat diet respectively. They revealed that high-fat salt sensitive rats showed endothelium-dependent relaxation due to acetylcholine. They conclude that diet-induced obesity can genetically protect from endothelial dysfunction.

The article presents a randomized study in individuals with the metabolic syndrome that indicated that nebivolol has a favorable effect on fibrin balance compared with meteorology. It also shows that nebivolol lacks negative effects on insulin sensitivity and oxidative stress. The article also hypothesizes that nebivolol have more favorable effects compared with an earlier-generation ß-blocker.

Defining heart failure (HF) is a matter of finding the most appropriate words to formulate the definiens for HF that will be universally applicable in all specific circumstances pertaining to the nature of HF. Currently available definitions of HF contain ambiguities and notable deficiencies such that non-heart failure medical conditions can become mislabelled as heart failure. Principles of how best to formulate definitions have been employed to provide a guide on how to appraise published definitions of HF. A fundamental requirement of a good definition is that it should be universal, and by this criterion, we need to question the validity of a conventional dogma that a collection of clinical diagnostic features are equivalent to HF definitions. A long-standing deficiency in HF definitions is the inability to take into account the quantifiable extent of functional impairment of the heart. Other traditional misconceptions surrounding HF definitions have also been addressed. In line with Derek Gibson's proposal, we have rephrased William Harvey's description of the cardiac role in maintaining the circulation in terms of Newtonian physics and of the Law of Conservation of Energy to reach a more universal and less ambiguous definition of HF, with the objective of advancing the science of HF and the treatment of this distressing condition. [ABSTRACT FROM AUTHOR]

Abstract: The renin–angiotensin system (RAS) plays a crucial role in cardiovascular and neuronal (patho-)physiology. The angiotensin AT2 receptor (AT2R) seems to counteract the proinflammatory, prohypertrophic and profibrotic actions of the AT1 receptor. Recently, we identified a novel protein, termed “AT2R binding protein” (ATBP/ATIP) which seems essential for AT2R-mediated growth inhibition. Poly(ADP-ribose) polymerase-1 (PARP-1) can act as a nuclear integrator of angiotensin II-mediated cell signalling, and has been implicated in the pathogenesis of cardiovascular and neuronal disease. In this study, promoters of human AT2R and ATIP1 were cloned and two transcriptional start sites in the ATIP1 promoter were identified whereas only one was detected in the AT2R promoter. Promoter assays indicated that the exon 1–intron 1 region of AT2R is necessary and sufficient for AT2R promoter activity. Inverse cloning experiments indicated that this regulatory region is a promoter but not an enhancer element implicating (a) further start site(s) in this region. Consistently, the exon 1–intron 1 region of AT2R was shown to tether the basal transcriptional machinery. Overexpression, pharmacological inhibition and ablation of PARP demonstrated that PARP-1 activates the ATIP1 gene but represses the AT2R on promoter and mRNA levels in vitro, and in brain tissue in vivo. Additional experiments indicated that AT2R activation does not modulate PARP-1 transcript levels but increases AT2R promoter activity, thereby creating a positive feedback mechanism. Our results demonstrate that PARP-1 acts as novel node within the RAS network based on its ability to regulate downstream targets such as AT2R and its adapter protein ATBP. [Copyright &y& Elsevier]

Cardiovascular pathophysiological changes, such as hypertension and enlarged ventricles, reflect the altered functions of the heart and its circulation during ill-health. This article examines the normal and altered anatomy of the cardiac valves, the contractile elements and enzymes of the myocardium, the significance of the different factors associated with cardiac output, and the role of the autonomic nervous system in the heart beat. It also explores how certain diseases alter these functions and result in cardiac symptoms. Nurses can benefit from knowledge of these specific changes, for example, by being able to ask relevant questions in order to ascertain the nature of a patient's condition, by being able to take an effective patient history and by being able to read diagnostic results, such as electrocardiograms and cardiac enzyme results. All this will help nurses to promote sound cardiac care based on a physiological rationale. [ABSTRACT FROM AUTHOR]

Abstract: Power spectrum analysis of cardiovascular signal variability, and in particular of the RR period (heart rate variability, HRV), is a widely used methodology for investigating autonomic neural regulation in health and disease that can quantify the sympathovagal balance modulating the sinus node pacemaker. In some cases, it can also quantify the neural regulation of other organs or apparatuses. However, use of the correct methodology is crucial to extract the information embedded in the frequency domain. In numerous abnormal conditions, such as essential arterial hypertension, acute myocardial infarction and heart failure, the sympathovagal balance may be altered in basal conditions. However, a reduced responsiveness to an excitatory stimulus is the most common feature that characterizes numerous pathophysiological states. The attenuation of an oscillatory pattern can also reflect an altered target function, thus providing important prognostic markers. The general features of this approach correspond well to the needs of an internist attempting to envisage the involvement of the whole organism in a disease process. [Copyright &y& Elsevier]

Extracellular vesicles are composed of loaded soluble substances and lipid bilayers; these include apoptotic bodies, exosomes, and microvesicles. Extracellular vesicles, as carriers of biological information between cells, have been recognized for their role in the diagnosis and treatment of cardiovascular diseases. The biogenesis of extracellular vesicles is closely related to autophagy. Moreover, extracellular vesicles further affect autophagy levels in target cells through their transmitted contents. Autophagy is a catabolic cell process that maintains cell homeostasis by eliminating misfolded proteins and damaged organelles. Existing studies have revealed that extracellular vesicles and autophagy share molecular mechanisms with notable crosstalk, including, perspectives such as amphisomes and "secretory autophagy." In this review, we first introduce the biogenesis of extracellular vesicles and the classic views of autophagy before moving onto the crosstalk between extracellular vesicles and autophagy. Finally, we discuss the research progress of extracellular vesicles and autophagy in cardiovascular pathophysiology. [ABSTRACT FROM AUTHOR]