Lack of right ventricular hypertrophy is associated with right heart failure in patients with left ventricular failure.

Presence of right heart failure (RHF) is associated with a worse prognosis in patients with left ventricular failure (LVF). While the cause of RHF secondary to LVF is multifactorial, an increased right ventricular (RV) afterload is believed as the major cause of RHF. However, data are scarce on the adaptive responses of the RV in patients with LVF. Our aim was to understand the relationship of right ventricular hypertrophy (RVH) with RHF and RV systolic and diastolic properties in patients with LVF. 55 patients with a left ventricular ejection fraction of 40% or less were included in the present study. A comprehensive two-dimensional transthoracic echocardiographic examination was done to all participants. 12 patients (21.8%) had RHF, and patients with RHF had a significantly lower right ventricular free wall thickness (RVFWT) as compared to patients without RHF (5.3 ± 1.7 mm vs. 6.6 ± 0.9 mm, p = 0.02) and the difference remained statistically significant after adjusting for confounders (Δx̅:1.34 mm, p = 0.002). RVFWT had a statistically significant correlation with tricuspid annular plane systolic excursion (r = 0.479, p < 0.001) and tricuspid annular lateral systolic velocity (r = 0.360, p = 0.007), but not with the indices of the RV diastolic function. None of the patients with concentric RVH had RHF, while 22.2% of patients with eccentric RVH and 66.7% of patients without RVH had RHF (p < 0.01 as compared to patients with concentric RVH). In patients with left ventricular systolic dysfunction, absence of RVH was associated with worse RV systolic performance and a significantly higher incidence of RHF.

Echocardiographic assessment in cardiogenic shock.

Echocardiography is the most helpful diagnostic modality in cardiogenic shock, the management of which still remains challenging despite advances in therapeutic options. The presence of cardiogenic shock portends high mortality rates. Therefore, rapid recognition, identification of the underlying cause, and evaluation of the severity of hemodynamic dysfunction are vital for correct management. Whether the cause of shock is unknown, suspected, or established, echocardiography is utilized in its diagnosis and management as well as to monitor progress. It is recommended as the modality of first choice. No other investigative bedside tool can offer comparable diagnostic capability, allowing for exact targeting of the underlying cardiac and hemodynamic problems. Echocardiography can promptly provide an impression of the etiology of shock and the potential line of treatment. Normal left ventricular and right ventricular systolic function, normal cardiac chamber dimensions, absence of any significant valvular pathology, and absence of any pericardial effusion virtually rule out a cardiac cause of shock. This review discusses the role of echocardiography as a decision-making tool in the evaluation and management of cardiogenic shock.

The Effect of Intracoronary Infusion of Autologous Bone Marrow-Derived Lineage-Negative Stem/Progenitor Cells on Remodeling of Post-Infarcted Heart in Patient with Acute Myocardial Infarction.

Introduction: Regenerative capacity of the heart is limited, and the post-infarct left ventricle (LV) dysfunction is associated with poor prognosis. Administration of stem/progenitor cells (SPCs) is a promising approach for cardiac regeneration. Objectives: In the study, we assessed LV function and post-infarcted remodeling in patients with ST-elevated myocardial infarct (STEMI) who received autologous lineage-negative (LIN-) SPCs. Patients and methods: Patients with STEMI and one-vessel coronary artery disease treated with percutaneous revascularisation were divided into study group (LIN- group, 15 patients) that received standard therapy and autologous BM-derived LIN- SPCs and control group (standard therapy group, 19 patients). The cells were administered intracoronary 24 hours after STEMI. The follow-up was 12 months with subsequent non-invasive tests and laboratory parameter evaluation on days 1st, 3rd, and 7th as well as at 1st, 3rd, 6th and 12th month after STEMI. Results: All procedures related to SPCs administration were well tolerated by the patients. In 12-month follow-up, there were no major adverse cardiac events connected with LIN- SPCs administration. During 12-month follow-up, 9 patients from LIN- group (Responders) achieved an improvement in LV ejection fraction (>10% after 12 months) with no signs of unfavorable LV remodeling. Laboratory parameters analysis showed that Troponin T levels were significantly lower until day 7th in the Responders group, while brain natriuretic peptide (BNP) level remained significantly lower from day 3rd to 12th month respectively. Conclusions: Intracoronary infusion of autologous BM-derived LIN- stem/progenitor cells is feasible and safe for patient. Improvement in LV function and prevention of unfavorable remodeling in the 60% of study group seems relatively promising. Stem cell-based therapy for cardiac regeneration still needs more accurate and extensive investigations to estimate and improve their efficacy.

Differences in Biomarkers Pattern Between Severe Isolated Right and Left Ventricular Dysfunction After Cardiac Surgery.

OBJECTIVE: To find out if there are any differences in biomarkers between severe isolated right ventricular (RV) dysfunction and severe isolated left ventricular (LV) dysfunction after cardiac surgery using cardiopulmonary bypass. DESIGN: Observational study. SETTING: Teaching hospital. PARTICIPANTS: A total of 46 patients who had severe isolated RV or LV dysfunction after cardiac surgery. INTERVENTION: The authors collected perioperative clinical and biomarker data. MEASUREMENTS AND MAIN RESULTS: Severe isolated RV dysfunction patients (n = 20) had higher postoperative direct bilirubin (p = 0.030), total bilirubin (p = 0.044), glucose (p = 0.011), and international normalized ratio (INR) (p = 0.050) by repeated measure analysis of variance when compared with patients with severe isolated LV dysfunction (n = 26). The RV group also showed lower preoperative alanine transferase (19.3 ± 1.5 v 32.7 ± 4.2, p = 0.001), higher 4-hour INR (1.5 ± 0.3 v 1.4 ± 0.2, p = 0.008), and higher 48-hour INR (1.8 ± 0.4 v 1.4 ± 0.1, p < 0.001). None in the LV group died, whereas 4 patients in the RV group died (all of them had preoperative atrial fibrillation and underwent double valve replacement surgery). CONCLUSION: The authors observed biomarkers differences between severe isolated RV dysfunction and severe isolated RV dysfunction.

Implantable Cardioverter Defibrillator Use in Males with Duchenne Muscular Dystrophy and Severe Left Ventricular Dysfunction.

Duchenne muscular dystrophy (DMD) is characterized by myocardial fibrosis and left ventricular (LV) dysfunction. Implantable cardioverter defibrillator (ICD) use has not been characterized in this population but is considered for symptomatic patients with severe LV dysfunction (SLVD) receiving guideline-directed medical therapy (GDMT). We evaluated ICD utilization and efficacy in patients with DMD. Retrospective cohort study of DMD patients from 17 centers across North America between January 2, 2005 and December 31, 2015. ICD use and its effect on survival were evaluated in patients with SLVD defined as ejection fraction (EF) < 35% and/ or shortening fraction (SF) < 16% on final echocardiogram. SLVD was present in 57/436 (13.1%) patients, of which 12 (21.1%) died during the study period. Of these 12, (mean EF 20.9 ± 6.2% and SF 13.7 ± 7.2%), 8 received GDMT, 5 received steroids, and none received an ICD. ICDs were placed in 9/57 (15.8%) patients with SLVD (mean EF 31.2 ± 8.5% and SF 10.3 ± 4.9%) at a mean age of 20.4 ± 6.3 years; 8/9 received GDMT, 7 received steroids, and all were alive at study end; mean ICD duration was 36.1 ± 26.2 months. Nine ICDs were implanted at six different institutions, associated with two appropriate shocks for ventricular tachycardia in two patients, no inappropriate shocks, and one lead fracture. ICD use may be associated with improved survival and minimal complications in DMD cardiomyopathy with SLVD. However, inconsistent GDMT utilization may be a significant confounder. Future studies should define optimal indications for ICD implantation in patients with DMD cardiomyopathy.

Altered myofilament structure and function in dogs with Duchenne muscular dystrophy cardiomyopathy.

AIM: Duchenne Muscular Dystrophy (DMD) is associated with progressive depressed left ventricular (LV) function. However, DMD effects on myofilament structure and function are poorly understood. Golden Retriever Muscular Dystrophy (GRMD) is a dog model of DMD recapitulating the human form of DMD. OBJECTIVE: The objective of this study is to evaluate myofilament structure and function alterations in GRMD model with spontaneous cardiac failure. METHODS AND RESULTS: We have employed synchrotron X-rays diffraction to evaluate myofilament lattice spacing at various sarcomere lengths (SL) on permeabilized LV myocardium. We found a negative correlation between SL and lattice spacing in both sub-epicardium (EPI) and sub-endocardium (ENDO) LV layers in control dog hearts. In the ENDO of GRMD hearts this correlation is steeper due to higher lattice spacing at short SL (1.9µm). Furthermore, cross-bridge cycling indexed by the kinetics of tension redevelopment (ktr) was faster in ENDO GRMD myofilaments at short SL. We measured post-translational modifications of key regulatory contractile proteins. S-glutathionylation of cardiac Myosin Binding Protein-C (cMyBP-C) was unchanged and PKA dependent phosphorylation of the cMyBP-C was significantly reduced in GRMD ENDO tissue and more modestly in EPI tissue. CONCLUSIONS: We found a gradient of contractility in control dogs' myocardium that spreads across the LV wall, negatively correlated with myofilament lattice spacing. Chronic stress induced by dystrophin deficiency leads to heart failure that is tightly associated with regional structural changes indexed by increased myofilament lattice spacing, reduced phosphorylation of regulatory proteins and altered myofilament contractile properties in GRMD dogs.

Systolic heart failure after liver transplantation: Incidence, predictors, and outcome.

Although most patients presenting for liver transplantation have normal left ventricular function, some develop left ventricular failure after transplantation. The primary objective of our study was to determine the predictors of systolic heart failure (HF) occurring immediately after liver transplantation. Its etiology, prospects of recovery, and factors associated with nonrecovery were also studied. Liver transplantations performed at our institution from January 2006 to February 2015 were evaluated using prospectively collected institutional registries. Patients with echocardiographically documented decline in ejection fraction to <45% within 6 months after liver transplantation were identified. Four controls were chosen per case: matched for age, gender, transplant year, and model for end-stage liver disease score. Conditional multivariable logistic regression was used for primary analysis and nonparametric tests for comparison between groups. In a cohort of 1284 adult patients, 45 cases and 180 controls were identified. Diastolic dysfunction (DD) was an independent predictor (OR 5.26, 95% CI 1.03-28.57, P = .04) of systolic HF in multivariable analysis. Stress-induced cardiomyopathy was the most common etiology. Left ventricular function recovered in 21 patients. Pretransplant DD decreased the chances of recovery (P = .05). In conclusion, patients with pretransplant DD need close post-transplant follow-up for timely identification of HF.

Why septal motion is a marker of right ventricular failure in pulmonary arterial hypertension: mechanistic analysis using a computer model.

Rapid leftward septal motion (RLSM) during early left ventricular (LV) diastole is observed in patients with pulmonary arterial hypertension (PAH). RLSM exacerbates right ventricular (RV) systolic dysfunction and impairs LV filling. Increased RV wall tension caused by increased RV afterload has been suggested to cause interventricular relaxation dyssynchrony and RLSM in PAH. Simulations using the CircAdapt computational model were used to unravel the mechanism underlying RLSM by mechanistically linking myocardial tissue and pump function. Simulations of healthy circulation and mild, moderate, and severe PAH were performed. We also assessed the effects on RLSM when PAH coexists with RV or LV contractile dysfunction. Our results showed prolonged RV shortening in PAH causing interventricular relaxation dyssynchrony and RLSM. RLSM was observed in both moderate and severe PAH. A negative transseptal pressure gradient only occurred in severe PAH, demonstrating that negative pressure gradient does not entirely explain septal motion abnormalities. PAH coexisting with RV contractile dysfunction exacerbated both interventricular relaxation dyssynchrony and RLSM. LV contractile dysfunction reduced both interventricular relaxation dyssynchrony and RLSM. In conclusion, dyssynchrony in ventricular relaxation causes RLSM in PAH. Onset of RLSM in patients with PAH appears to indicate a worsening in RV function and hence can be used as a sign of RV failure. However, altered RLSM does not necessarily imply an altered RV afterload, but it can also indicate altered interplay of RV and LV contractile function. Reduction of RLSM can result from either improved RV function or a deterioration of LV function.NEW & NOTEWORTHY A novel approach describes the mechanism underlying abnormal septal dynamics in pulmonary arterial hypertension. Change in motion is not uniquely induced by altered right ventricular afterload, but also by altered ventricular relaxation dyssynchrony. Extension or change in motion is a marker reflecting interplay between right and left ventricular contractility.

Low-dose intensive insulin therapy in patients with Acute Coronary Syndrome accompanied by Left Ventricular Failure: audit of two UK hospitals.

AIMS AND OBJECTIVES: To determine whether a low-dose intravenous insulin regimen reduces blood glucose levels at a timely rate and associated side effects among patients with Acute Coronary Syndrome and Left Ventricular Failure. BACKGROUND: Induced hypoglycaemia and the associated risks have questioned the benefits of intensive insulin therapy in patients presenting with raised blood glucose levels and Acute Coronary Syndromes. Local audit data identified that patients with Acute Coronary Syndrome and Left Ventricular Failure experienced more hypoglycaemic episodes than those with Acute Coronary Syndrome alone. Consequently, a new regimen of low-dose insulin for this group was implemented and audited over 12 months. DESIGN: Audit. METHODS: Thirty-six consecutive patient notes with a diagnosis of Acute Coronary Syndrome and blood glucose of ≥10 mmol/l treated with a new insulin therapy regimen were analysed. Data were extracted using a standardised form and entered into an Excel spreadsheet for analysis. RESULTS: The mean age of the sample was 70 years with 66% of subjects being men and 50% presenting with Acute Coronary Syndrome and Left Ventricular Failure. The low-dose regimen was effective in achieving normoglycaemia, (range 4-8 mmol/l) for a consecutive six-hour period. This was achieved in 72% of patients and within a median time of 13 hours. CONCLUSION: The audit suggests that a low-dose insulin regimen can effectively stabilise blood glucose in patients presenting with both Acute Coronary Syndrome and Left Ventricular Failure. The importance of regularly monitoring blood sugar levels is vital and highlights the role of nurses in minimising patient risk and promoting safety. RELEVANCE TO PRACTICE: Nurses are instrumental in the safe implementation of intensive insulin guidelines. Close monitoring of patients is essential, enabling timely adjustments to treatments and ensuring patient safety. Regular audits allow nurses to evaluate care provision and continue to drive practice forward.

Management of three cardiogenic pulmonary edemas occurring in a patient scheduled for left ventricular assist device implantation: indicators for determining left ventricular assist device pump speed.

A male patient with Marfan syndrome underwent aortic root replacement and developed left ventricular (LV) failure. Four years later, he underwent aortic arch and aortic valve replacement. Thereafter, his LV failure progressed, and cardiogenic pulmonary edema (CPE) appeared, which we treated with extracorporeal LV assist device (LVAD) placement. Three months later, the patient developed aspiration pneumonia, which caused hyperdynamic right ventricle (RV) and CPE. We treated by changing his pneumatic LVAD to a high-flow centrifugal pump. A month later, he underwent thoracoabdominal aortic replacement. After four weeks, he developed septic thrombosis and LVAD failure, which caused CPE. We treated with LVAD circuit replacement and an additional membrane oxygenator. Four months later, he underwent DuraHeart(®) implantation. During this course, pulmonary artery wedge pressure (PAWP) varied markedly. Additionally, systolic pulmonary artery pressure (sPAP), left atrial diameter (LAD), RV end-diastolic diameter (RVEDD) and estimated RV systolic pressure (esRVP) changed with PAWP changes. In this patient, LV failure and hyperdynamic RV caused the CPEs, which we treated by adjusting the LVAD output to the RV output. Determining LVAD output, RV function and LV end-diastolic diameter are typically referred, and PAWP, LAD, RVEDD, and sPAP could be also referred.

Management of acute heart failure in the emergency department.

Acute heart failure (AHF) is a leading cause of hospital admission in the UK and is associated with significant mortality. The National Institute for Health and Care Excellence ( 2014 ) has published guidelines for the management of AHF but, after a clinical event in which a patient's management differed from that recommended in the guidelines occurred in the author's emergency department, he conducted a critical analysis of them. This article provides a case study of the clinical event, reviews the treatment methods adopted and explores the rationale for taking a different approach from that recommended in the guidelines. The evidence base for the use of diuretics, nitrates and non-invasive ventilation in the management of patients with AHF is also appraised.

ProtekDuo percutaneous ventricular support system-physiology and clinical applications.

The ProtekDuo (LivaNova, London, UK) cannula is a dual-lumen device, typically inserted into the right internal jugular (IJ) vein through a percutaneous approach, with fluoroscopy or ultrasound guidance. When connected to a pump, such as the TandemHeart (LivaNova, London, UK) or CentriMag (Abbott, Pleasanton, CA, USA), it can function as a right ventricular (RV) mechanical circulatory support (MCS). When an oxygenator is also added [veno-pulmonary (V-P)], it can provide extracorporeal membrane oxygenation (ECMO) support. This review aims to provide a comprehensive overview of the device's physiology and clinical applications. In the setting of RV failure (RVF), the ProtekDuo cannula, with its outflow in the main pulmonary artery (PA), can bypass the failing RV, improving pulmonary flow, left atrial (LA) filling pressures, and left ventricular (LV) preload. This can also reduce ventricular interdependence and leftward shift of the interventricular septum that occurs in RVF. In this review, the key sections expand on the use of the ProtekDuo cannula in the management of critically ill patients, specifically, the use of ProtekDuo for RV myocardial infarction (MI) RVF, LV assist device (LVAD) implantation-associated RVF, RVF post-heart transplantation, temporary biventricular MCS as bridge to recovery (ECpella 2.0 or PROpella), biventricular support as bridge to recovery or decision, isolated LV failure, post lung transplantation (LT) care, and other miscellaneous clinical scenarios. ProtekDuo is an important tool in the armory of RVF management. The ProtekDuo system is expected to gain more popularity given its clear advantages such as groin-free approach allowing for mobility, easy percutaneous deployment, compatibility with various pumps and oxygenators, and the versatility to be integrated in numerous configurations. In an era of expanding MCS options, further research is needed to better understand the optimal tool for specific patient subsets.

Septic cardiomyopathy phenotype in the critically ill may depend on antimicrobial resistance.

Background: Sepsis is a life-threatening organ dysfunction, and septic cardiomyopathy (SCM) may complicate the course of the disease. Infection with multidrug-resistant (MDR) pathogens has been linked with worse outcomes. This study aims to evaluate SCM in patients with infections caused by different antimicrobial-resistant phenotypes. Method: This retrospective study included patients with sepsis/septic shock, hospitalized, and intubated in the intensive care unit of the University Hospital of Larissa between January 2022 and September 2023 with echocardiographic data during the first two days after infection onset. The patients were divided into two groups: non-MDR-SCM group and MDR-SCM group. The cardiac function was compared between the two groups. Result: A total of 62 patients were included in the study. Forty-four patients comprised the MDR-SCM and 18 the non-MDR-SCM group. Twenty-six patients (41.9%) presented with left ventricular (LV) systolic dysfunction, and ≤35% right ventricular fractional area change (RVFAC) was present in 56.4%. LV systolic function was more severely impaired in the non-MDR-SCM group (left ventricular ejection fraction, 35.8% ±4.9% vs. 45.6%±2.4%, P=0.049; LV outflow tract velocity time integral, [10.1±1.4] cm vs. [15.3±0.74] cm, P=0.001; LV-Strain, -9.02%±0.9% vs. -14.02%±0.7%, P=0.001). The MDR-SCM group presented with more severe right ventricular (RV) dilatation (right ventricular end-diastolic area/left ventricular end-diastolic area, 0.81±0.03 vs. 0.7±0.05, P=0.042) and worse RV systolic function (RVFAC, 32.3%±1.9% vs. 39.6%±2.7%, P=0.035; tricuspid annular plane systolic excursion, [15.9±0.9] mm vs. [18.1±0.9] mm, P=0.165; systolic tissue Doppler velocity measured at the lateral tricuspid annulus, [9.9±0.5] cm/s vs. [13.1±0.8] cm/s, P=0.002; RV-strain, -11.1%±0.7% vs. -15.1%±0.9%, P=0.002). Conclusion: SCM related to MDR infection presents with RV systolic dysfunction predominance, while non-MDR-SCM is mainly depicted with LV systolic dysfunction impairment.

An updated review of experimental rodent models of pulmonary hypertension and left heart disease.

Left heart disease (LHD) is the leading cause of pulmonary hypertension (PH). Its recent growth has not been matched by the design of therapeutic agents directly targeting the disease. Effective therapies approved for pulmonary arterial hypertension (PAH) have been shown to be inefficient in patients with PH-LHD. Hence, there is a need for an animal model that would closely mimic PH-LHD in preclinical experiments. The current study describes and compares a number of rodent models of left ventricular failure and their potential to induce PH. It also evaluates whether, and to what extent, common PH models could develop LV failure. Articles were identified in the Pubmed/Medline and Web of Science online electronic databases following the PRISMA Protocol between 1992 and 2022. Quality assessment was carried out using the SYRCLE risk-of-bias tool for animal studies. Publication bias across studies using Egger's regression test statistic, was performed together with sensitivity analysis. A wide spectrum of protocols-135 studies and 207 interventions, was examined, including systemic hypertensive models, pressure-overload-induced HF, model of ischemic heart failure, and metabolic approaches based on high fat diet or metabolic syndrome. The most pronounced alterations in PH-related parameters were demonstrated for the common PH models, but were also seen in animals with LV failure induced by ischemic conditions, pressure overload or metabolic conditions. Models based on aortic banding, transverse aortic constriction (TAC), or with myocardial infarction (MI) caused by coronary artery ligation, demonstrated more pronounced worsening in PH due to LV failure; however, they also demonstrated poor survival, especially the ischemic-HF model. Common PH models, excluding prolonged exposure to monocrotaline, do not promote LV hypertrophy. Prolonged exposure to a high-fat diet, or a two-hit model of an obese ZSF1 rat combined with SU5416-induced pulmonary endothelial impairment (a VEGF receptor antagonist) worsened PH and impaired diastolic dysfunction. Due to the limited number of protocols, further trials are needed to confirm the utility of such approaches for modeling PH in subjects with metabolic syndrome. This would provide a clearer insight into the complexity of LHD, PH and metabolic disorders in PH-LHD, and thus accelerate the development of new therapies in clinical trials.

Development of the Modern Cardiothoracic Intensive Care Unit and Current Management.

The modern cardiothoracic intensive care unit (CTICU) developed as a result of advances in critical care, cardiology, and cardiac surgery. Patients undergoing cardiac surgery today are sicker, frailer, and have more complex cardiac and noncardiac morbidities. CTICU providers need to understand postoperative implications of different surgical procedures, complications that can occur in CTICU patients, resuscitation protocols for cardiac arrest, and diagnostic and therapeutic interventions such as transesophageal echocardiography and mechanical circulatory support. Optimum CTICU care requires a multidisciplinary team with collaboration between cardiac surgeons and critical care physicians with training and experience in the care of CTICU patients.

Therapeutic Development of Levosimendan in Acute and Advanced Heart Failure: A Systematic Review.

Levosimendan (LS) has been progressively used for the treatment of patients developing acute as well as chronic or advanced cardiac dysfunction. It has proven to be a better inotropic agent than its counterparts in terms of its ability to increase the cardiac output in an acutely or chronically decompensated heart without an increase in the myocardial oxygen demand. The purpose of this systematic review, which was carried out in accordance with Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) 2020, was to determine the efficacy and advantages of utilizing LS in patients with both acute and chronic heart failure. We collected and reviewed articles, including clinical trials, literature reviews, randomized and non-randomized control trials, case-control and cohort studies, and systematic reviews and meta-analyses published between January 1, 2012, and November 27, 2022. The databases that were used to collect these articles included Pubmed, Pubmed Central, Cochrane Library, and Google Scholar. After applying appropriate filters, a total of 143 reports were identified from these four databases. They were further screened and subjected to quality assessment tools which finally yielded 21 studies that were included in this systematic review. This review provides strong evidence that the pharmacological properties and different mechanisms of action of LS give it an upper hand over other inotropic agents for its successful administration in patients with either acute or advanced cardiac failure, which consists of left as well as right ventricular failure, either individually or in combination.

GENDER DIFFERENCES IN THE CLINICAL PROFILE AND SOCIODEMOGRAPHIC CHARACTERISTICS OF DILATED CARDIOMYOPATHY IN IBADAN, NIGERIA.

Background: Cardiomyopathies contribute about 18.2-40.2% (average- 21.4%) to the global burden of heart failure of which dilated cardiomyopathy (DCM) is a major cause. DCM is the second commonest cause of heart failure in Ibadan. The gender differences in the clinical profile has not been described in our setting. Objective: In this study, we set out to describe the gender differences in the pattern and presentation of DCM at the University College Hospital, Ibadan, Nigeria. Methods: This was an analysis of a prospectively collected data over a period of 5 years (August 1, 2016 to July 31, 2021). Results: A total of 117 subjects, 88 males (75.3%) and 29 females (24.8%) aged 50.30 ± 14.7 years (range, 17 to 86 years). Males had significantly achieved a higher educational level than females (p = 0.004). Males were more likely to be employed and had more monthly income compared to females. Males were significantly more likely to use alcohol and smoke cigarette (p = 0.0001 and 0.001 respectively). Females were more likely to be in NYHA class III/IV. There was no statistically significant difference in the relationship between any medication and gender of participants (p > 0.05). Conclusions: DCM is a disease of young and middle-aged adults in our population. The commonest age group was 20-39 years and there was male preponderance. There were some gender differences in the clinical profile of the disease in our environment.

Animal models of pulmonary hypertension due to left heart disease.

Pulmonary hypertension due to left heart disease (PH-LHD) is regarded as the most prevalent form of pulmonary hypertension (PH). Indeed, PH is an independent risk factor and predicts adverse prognosis for patients with left heart disease (LHD). Clinically, there are no drugs or treatments that directly address PH-LHD, and treatment of LHD alone will not also ameliorate PH. To target the underlying physiopathological alterations of PH-LHD and to develop novel therapeutic approaches for this population, animal models that simulate the pathophysiology of PH-LHD are required. There are several available models for PH-LHD that have been successfully employed in rodents or large animals by artificially provoking an elevated pressure load on the left heart, which by transduction elicits an escalated pressure in pulmonary artery. In addition, metabolic derangement combined with aortic banding or vascular endothelial growth factor receptor antagonist is also currently applied to reproduce the phenotype of PH-LHD. As of today, none of the animal models exactly recapitulates the condition of patients with PH-LHD. Nevertheless, the selection of an appropriate animal model is essential in basic and translational studies of PH-LHD. Therefore, this review will summarize the characteristics of each PH-LHD animal model and discuss the advantages and limitations of the different models.