PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

hypertrophy, left ventricular - Top 30 Publications

Diagnostic accuracy of multi-lead ECGs obtained using a pocket-sized bipolar handheld event recorder.

Handheld ECG event recorders are useful for rhythm monitoring but only record a single lead, which may limit interpretation. We sought to investigate if a multi-lead ECG may be reconstituted using this device, and aimed to evaluate diagnostic accuracy.

Systemic inflammation is associated with myocardial fibrosis, diastolic dysfunction, and cardiac hypertrophy in patients with hypertrophic cardiomyopathy.

Regional or diffuse fibrosis is an early feature of hypertrophic cardiomyopathy (HCM) and is related to poor prognosis. Previous studies have documented low-grade inflammation in HCM. The aim of this study was to examine the relationships between circulating inflammatory markers and myocardial fibrosis, systolic and diastolic dysfunction, and the degree of cardiac hypertrophy in HCM patients.

Prevalence and Clinical Characteristics of Refractory Hypertension.

We aimed to estimate the prevalence of refractory hypertension (RfH) and to determine the clinical differences between these patients and resistant hypertensives (RH). Secondly, we assessed the prevalence of white-coat RfH and clinical differences between true- and white-coat RfH patients.

Improvement in the sensitivity of newborn screening for Fabry disease among females through the use of a high-throughput and cost-effective method, DNA mass spectrometry.

Many female carriers of Fabry disease are likely to develop severe morbidity and mortality. However, by our own estimation, around 80% of female newborns are missed by our current enzyme-based screening approach. Our team's aim was to develop an improved cost-effective screening method that is able to detect Fabry disease among female newborns. In Taiwan, based on a database of 916,000 newborns, ~98% of Fabry patients carry mutations out of a pool of only 21 pathogenic mutations. An Agena iPLEX platform was designed to detect these 21 pathogenic mutations using only a single-assay panel. A total of 54,791 female infants were screened and 136 female newborns with the IVS4 + 919G > A mutation and one female newborn with the c.656T > C mutation were identified. Using the current enzyme-based newborn screening approach as baseline, around 83% of female newborns are being missed. Through a family study of the IVS4 female newborns, 30 IVS4 adult family members were found to have left ventricular hypertrophy. Ten patients received endomyocardial biopsy and all were found to have significant globotriaosylceramide (Gb3) accumulation in their cardiomyocytes. All of these individuals now receive enzyme replacement therapy. We have demonstrated that the Agena iPLEX assay is a powerful tool for detecting females with Fabry disease. Furthermore, through this screening, we also have been able to identify many disease-onset adult family members who were originally undiagnosed for Fabry disease. This screening helps them to receive treatment in time before severe and irreversible cardiac damage has occurred.

Hyperoxia-induced cardiotoxicity and ventricular remodeling in type-II diabetes mice.

Hyperoxia, or supplemental oxygen, is regularly used in the clinical setting for critically ill patients in ICU. However, several recent studies have demonstrated the negative impact of this treatment in patients in critical care, including increased rates of lung and cardiac injury, as well as increased mortality. The purpose of this study was to determine the predisposition for arrhythmias and electrical remodeling in a type 2 diabetic mouse model (db/db), as a result of hyperoxia treatment. For this, db/db and their heterozygous controls were treated with hyperoxia (> 90% oxygen) or normoxia (normal air) for 72-h. Immediately following hyperoxia or normoxia treatments, mice underwent surface ECG. Excised left ventricles were used to assess ion channel expression, including for Kv1.4, Kv1.5, Kv4.2, and KChIP2. Serum cardiac markers were also measured, including cardiac troponin I and lactate dehydrogenase. Our results showed that db/db mice have increased sensitivity to arrhythmia. Normoxia-treated db/db mice displayed features of arrhythmia, including QTc and JT prolongation, as well as QRS prolongation. A significant increase in QRS prolongation was also observed in hyperoxia-treated db/db mice, when compared to hyperoxia-treated heterozygous control mice. Db/db mice were also shown to exhibit ion channel dysregulation, as demonstrated by down-regulation in Kv1.5, Kv4.2, and KChIP2 under hyperoxia conditions. From these results, we conclude that: (1) diabetic mice showed distinct pathophysiology, when compared to heterozygous controls, both in normoxia and hyperoxia conditions. (2) Diabetic mice were more susceptible to arrhythmia at normal air conditions; this effect was exacerbated at hyperoxia conditions. (3) Unlike in heterozygous controls, diabetic mice did not demonstrate cardiac hypertrophy as a result of hyperoxia. (4) Ion channel remodeling was also observed in db/db mice under hyperoxia condition similar to its heterozygous controls.

Cardiac deformation imaging.

Deformation imaging (strain imaging) is an echocardiographic method for evaluating myocardial function that is also suitable for clinical use. There are two deformation imaging techniques: Tissue Doppler and 2D strain (speckle tracking). Deformation imaging allows the measurement of regional myocardial deformation in three dimensions. Longitudinal deformation (strain) measures longitudinal myocardial fiber contraction, and reflects subendocardial myocardial function, which is usually the first to deteriorate in patients with heart disease. Reduced longitudinal strain can reveal heart disease even when ejection fraction and cardiac contractility appear normal. Deformation imaging can be used for diagnosing ischemia, distinguishing between pathological and physiological hypertrophy, and early detection of heart disease in hypertension or diabetes. Global longitudinal strain (GLS) is an indicator of overall left ventricular systolic function, and correlates with the prognosis better than ejection fraction.

Feasibility and reproducibility of feature-tracking-based strain and strain rate measures of the left ventricle in different diseases and genders.

The measurement of myocardial deformation by strain analysis is an evolving tool to quantify regional and global myocardial function.

The Association Between Myocardial Fibrosis and Depressed Capillary Density in Rat Model of Left Ventricular Hypertrophy.

Myocardial fibrogenesis is initiated once the coordination between oxygen supply and demand is disrupted in pressure overload-induced cardiac hypertrophy. Clinical observations showed that myocardial fibrosis did not evenly occur in the hypertrophic myocardium. The present study was undertaken to specifically address differential vulnerabilities to fibrogenesis of different regions in the myocardium subjected to pressure overload-induced hypertrophy. SD rats were divided into two groups, sham-operated control and ascending artery constriction-induced cardiac hypotrophy. Thirty-four weeks after surgery, rats were sacrificed and hearts were harvested. Myocardial tissues were processed and sequentially sectioned for detection of collagen deposition, myocyte hypertrophy and vascular density analysis. Redundant collagen stained with Sirius red and anti-collagen I antibody was found in the extracellular matrix, but high volume of collagen fraction was largely localized more in posterior and lateral walls than in anterior wall and interventricular septum, which is in accordance with the accumulation of fibroblasts. In association with the differential regional collagen accumulation, the cardiomyocytes were more hypertrophic in the posterior and lateral wall than the other left ventricle. However, the capillary density in the lateral and posterior walls was significantly decreased. The results indicated that the posterior and lateral walls were more vulnerable to fibrogenesis post-pressure overload-induced cardiac hypertrophy, which was associated with the depressed angiogenesis in these two regions.

Roles and Mechanisms of Herbal Medicine for Diabetic Cardiomyopathy: Current Status and Perspective.

Diabetic cardiomyopathy is one of the major complications among patients with diabetes mellitus. Diabetic cardiomyopathy (DCM) is featured by left ventricular hypertrophy, myocardial fibrosis, and damaged left ventricular systolic and diastolic functions. The pathophysiological mechanisms include metabolic-altered substrate metabolism, dysfunction of microvascular, renin-angiotensin-aldosterone system (RAAS) activation, oxidative stress, cardiomyocyte apoptosis, mitochondrial dysfunction, and impaired Ca2+ handling. An array of molecules and signaling pathways such as p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK), and extracellular-regulated protein kinases (ERK) take roles in the pathogenesis of DCM. Currently, there was no remarkable effect in the treatment of DCM with application of single Western medicine. The myocardial protection actions of herbs have been gearing much attention. We present a review of the progress research of herbal medicine as a potential therapy for diabetic cardiomyopathy and the underlying mechanisms.

Detection of Urinary Mulberry Bodies Leads to Diagnosis of Fabry Cardiomyopathy: A Simple Clue in the Urine Sediment.

The Clinical Usefulness of Measurement of Visceral Fat Area Using Multi-Frequency Bioimpedance: The Association with Cardiac and Renal Function In General Population with Relatively Normal Renal Function.

Background: This study was performed to determine the clinical usefulness of measurement of visceral fat area (VFA) using bioimpedance analysis in relation with left ventricular hypertrophy (LVH), diastolic dysfunction parameters, and decreased estimated glomerular filtration rate (eGFR). Methods: A cross-sectional analysis was performed on 1028 patients with eGFR≥60 ml/min/1.73m2, aged 40 - 64 years, and who underwent routine health check-ups. Subjects were divided into tertiles based on their VFA. Associations of VFA with echocardiographic parameters and eGFR were evaluated. Results: Across the VFA teriltes, there was a significant trend for increasing left ventricular mass index (LVMi), left atrial diameter (LAD), and ratio of early mitral inflow velocity to peak mitral annulus velocity (E/E' ratio) and that for decreasing ratio of early to late mitral inflow peak velocities (E/A ratio) and eGFR. In multivariate linear regression analysis, log-transformed VFA was significantly associated with increased LVMi, LAD, and E/E' ratio, and with decreased E/A ratio and eGFR. After adjustment for body mass index, log-transformed VFA remained as a significant determinant for E/A ratio. Conclusion: VFA may be associated with LV structure and diastolic function, and decreased eGFR in middle-aged adults with normal or mildly impaired renal function.

The Development of Left Ventricular Hypertrophy in Patients With Left-Sided Obstructive Lesions: Are Genetics at Play?

Ineffective and prolonged apical contraction is associated with chest pain and ischaemia in apical hypertrophic cardiomyopathy.

To investigate the hypothesis that persistence of apical contraction into diastole is linked to reduced myocardial perfusion and chest pain.

Coexistence of left ventricular hypertrophy and noncompaction: a case report.

Cardiac myosin-binding protein C is a novel marker of myocardial injury and fibrosis in aortic stenosis.

Cardiac myosin-binding protein C (cMyC) is an abundant sarcomeric protein and novel highly specific marker of myocardial injury. Myocyte death characterises the transition from hypertrophy to replacement myocardial fibrosis in advanced aortic stenosis. We hypothesised that serum cMyC concentrations would be associated with cardiac structure and outcomes in patients with aortic stenosis.

Differential cardiac hypertrophy and signaling pathways in pressure versus volume overload.

Mechanical overload can be classified into pressure overload and volume overload, causing concentric and eccentric cardiac hypertrophy, respectively. Here, we aimed to differentiate the load-mediated signaling pathways involved in pressure versus volume overload cardiac hypertrophy.

Ivabradine improves left ventricular twist and untwist during chronic hypertension.

Left ventricular (LV) dysfunction develops during LV hypertrophy and particularly during tachycardia. Thus we investigated the effects of heart rate (HR) reduction with ivabradine, an If-channel blocker, on LV twist and untwist which represents myocardial deformation occurring during the overall systole and diastole and therefore provide valuable evaluation of global LV systolic and diastolic function.

Responses of PKCε to cardiac overloads on myocardial sympathetic innervation and NET expression.

Protein kinase C (PKC) is a key mediator of many diverse physiological and pathological responses. PKC activation play an important regulatory role of cardiac function. The present study was performed to investigate whether there were differential activations of the PKCε and how the activation coupled with norepinephrine transporter (NET) surface expression, sympathetic innervation pattern and extracellular matrix remodeling in different cardiac hemodynamic overloads induced by abdominal aortic constriction or aortocaval fistula. At 8weeks after the operations, heart failure were induced, accompanied with myocardial hypertrophy, which was more pronounced in pressure overload (POL) than that of volume overload (VOL) rats, left ventricular dysfunction and increased plasma norepinephrine (NE). In POL rats there was an increase in myocardial collagen deposition, in contrast, the amount decreased in VOL as compared with the sham rats. POL remarkably upregulated PKCε membrane-cytosol ratio and downregulated NET membrane fraction, whereas, in VOL induced opposite changes. Accompanied with the PKCε activation, nerve sprouting, evidenced by myocardial GAP43 protein increased, and different nerve phenotypes were found, in POL tyrosine hydroxylase (TH) positive nerve density increased with NET and choline acetyltransferase (ChAT) immunoreactivity density decreased, in contrast, in VOL NET and ChAT increased, TH did not change. The overloads did not induce alteration of NET mRNA expression, but resulted in different myocardial β1-AR mRNA expression, in POL β1-AR mRNAwas significantly downregulated, while in VOL rats unaltered. Conclusion, the present results suggested that the different cardiac hemodynamic overload could differentially activate a common signaling, PKCε intermediate and thereby generate biological diversity.

Endogenous Annexin-A1 Regulates Haematopoietic Stem Cell Mobilisation and Inflammatory Response Post Myocardial Infarction in Mice In Vivo.

Endogenous anti-inflammatory annexin-A1 (ANX-A1) plays an important role in preserving left ventricular (LV) viability and function after ischaemic insults in vitro, but its long-term cardioprotective actions in vivo are largely unknown. We tested the hypothesis that ANX-A1-deficiency exaggerates inflammation, haematopoietic stem progenitor cell (HSPC) activity and LV remodelling in response to myocardial ischaemia in vivo. Adult ANX - A1 -/- mice subjected to coronary artery occlusion exhibited increased infarct size and LV macrophage content after 24-48 h reperfusion compared with wildtype (WT) counterparts. In addition, ANX - A1 -/- mice exhibited greater expansion of HSPCs and altered pattern of HSPC mobilisation 8 days post-myocardial infarction, with increased circulating neutrophils and platelets, consistent with increased cardiac inflammation as a result of increased myeloid invading injured myocardium in response to MI. Furthermore, ANX - A1 -/- mice exhibited significantly increased expression of LV pro-inflammatory and pro-fibrotic genes and collagen deposition after MI compared to WT counterparts. ANX-A1-deficiency increased cardiac necrosis, inflammation, hypertrophy and fibrosis following MI, accompanied by exaggerated HSPC activity and impaired macrophage phenotype. These findings suggest that endogenous ANX-A1 regulates mobilisation and differentiation of HSPCs. Limiting excessive monocyte/neutrophil production may limit LV damage in vivo. Our findings support further development of novel ANX-A1-based therapies to improve cardiac outcomes after MI.

Progressive impairment of atrial myocyte function during left ventricular hypertrophy and heart failure.

Hypertensive heart disease (HHD) can cause left ventricular (LV) hypertrophy and heart failure (HF). It is unclear, though, which factors may contribute to the transition from compensated LV hypertrophy to HF in HHD. We hypothesized that maladaptive atrial remodeling with impaired atrial myocyte function would occur in advanced HHD and may be associated with the emergence of HF. Experiments were performed on atrial myocytes and tissue from old (15-25months) normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) with advanced HHD. Based on the absence or presence of elevated lung weight, a sign of lung congestion and heart failure, SHR were divided into a non-failing (SHR-NF) and failing (SHR-HF) group. Compared with WKY, SHR exhibited elevated blood pressure, LV hypertrophy and left atrial (LA) hypertrophy with increased LA expression of markers of hypertrophy and fibrosis. SHR-HF were distinguished from SHR-NF by aggravated hypertrophy and fibrosis. SHR-HF atrial myocytes exhibited reduced contractility and impaired SR Ca2+ handling. Moreover, in SHR the expression and phosphorylation of SR Ca2+-regulating proteins (SERCA2a, calsequestrin, RyR2 and phospholamban) showed negative correlation with increasing lung weight. Increasing stimulation frequency (1-2-4Hz) of atrial myocytes caused a progressive increase in arrhythmogenic Ca2+ release (including alternans), which was observed most frequently in SHR-HF. Thus, in old SHR with advanced HHD there is profound structural and functional atrial remodeling. The occurrence of HF in SHR is associated with LA and RA hypertrophy, increased atrial fibrosis, impaired atrial myocyte contractility and SR Ca2+ handling and increased propensity for arrhythmogenic Ca2+ release. Therefore, functional remodeling intrinsic to atrial myocytes may contribute to the transition from compensated LV hypertrophy to HF in advanced HHD and an increased propensity of atrial arrhythmias in HF.

Mechanical deformation in adult patients with unrepaired aortic coarctation.

Aortic coarctation is a congenital heart disease that causes an increased left ventricular afterload, resulting in increased systolic parietal tension, compensatory hypertrophy, and left ventricular systolic and diastolic dysfunction. The speckle tracking is a new echocardiographic technique that allows the detection of subclinic left ventricular systolic dysfunction. The aim of this study was to detect early left ventricular dysfunction using mechanical deformation by echocardiography in adults with un-repaired aortic coarctation. A total of 41 subjects were studied, 20 patients with aortic coarctation and 21 control subjects, 21 women (51.2%), with an average age of 30 ± 10 years. All patients with aortic coarctation had systemic arterial hypertension (p < 0.001). Seventy percent (14/20) of the patients had bicuspid aortic valve. Statistically significance (p < 0.005) were found in left ventricular mass index, E/e ratio, pulmonary artery systolic pressure and peak velocity and maximum gradient of the aortic valve. The global longitudinal deformation of the left ventricle in patients with aortic coarctation was significative decreased, p < 0.001. The ejection fraction and the global longitudinal deformation of the left ventricle were significantly lower in patients with aortic coarctation compared to the control group, p < 0.003, p < 0.001, respectively. The subgroup of patients with coarctation and left ventricular ejection fraction < 55% had a marked decrease in global longitudinal strain (- 15.9 ± 4%). The radial deformation was increased in patients with aortic coarctation and showed a trend to be significant (r = 0.421; p < 0.06). A significant negative correlation was observed between the global longitudinal deformation and left ventricular mass index (r = 0.54; p = 0.01) in the aortic coarctation group. The patients with aortic coarctation and left ventricular hypertrophy had marked reduction of left ventricular global longitudinal deformation (- 16%, p < 0.05). In our study patients with normal left ventricular ejection fraction had abnormal global longitudinal deformation and also the increased left ventricular mass was related with a decreased left ventricular global longitudinal deformation as a sign of subclinical systolic dysfunction.

Local sympathetic denervation attenuates myocardial inflammation and improves cardiac function after myocardial infarction in mice.

Cardiac inflammation has been suggested to be regulated by the sympathetic nervous system (SNS). However, due to the lack of methodology to surgically eliminate the myocardial SNS in mice, neuronal control of cardiac inflammation remains ill defined. Here, we report a procedure for local cardiac sympathetic denervation in mice and tested its effect in a mouse model of heart failure post myocardial infarction.

Un-sweetening the Heart: Possible pleiotropic effects of SGLT2 inhibitors on cardio and cerebrovascular alterations in resistant hypertensive subjects.

Resistant hypertension is a multifactorial disease associated with several target organ damage, such as microalbuminuria, left ventricular hypertrophy and arterial stiffness. These subjects have high cardiovascular complications, especially when associated with diabetes condition. SGLT-2 inhibitors represent a new class of oral antidiabetic drugs that have shown positive effects in diabetics and even hypertensives subjects. Several studies demonstrated positive outcomes related to blood pressure levels, body weight and glycemic control. Also found a reduction on microalbuminuria, cardiac and arterial remodeling process and decrease in hospitalization care due heart failure. Despite these positive effects, the outcomes found for stroke were conflicted and tend neutral effect. Based on this, we sought to assess the pleiotropic effects of SGLT-2 inhibitors and the possible impact in resistant hypertension subjects. In order to analyze the prospects of SGLT-2 inhibitors as a possible medication to complement the therapy manage of this high risk class of patients.

A Feline HFpEF Model with Pulmonary Hypertension and Compromised Pulmonary Function.

Heart Failure with preserved Ejection Fraction (HFpEF) represents a major public health problem. The causative mechanisms are multifactorial and there are no effective treatments for HFpEF, partially attributable to the lack of well-established HFpEF animal models. We established a feline HFpEF model induced by slow-progressive pressure overload. Male domestic short hair cats (n = 20), underwent either sham procedures (n = 8) or aortic constriction (n = 12) with a customized pre-shaped band. Pulmonary function, gas exchange, and invasive hemodynamics were measured at 4-months post-banding. In banded cats, echocardiography at 4-months revealed concentric left ventricular (LV) hypertrophy, left atrial (LA) enlargement and dysfunction, and LV diastolic dysfunction with preserved systolic function, which subsequently led to elevated LV end-diastolic pressures and pulmonary hypertension. Furthermore, LV diastolic dysfunction was associated with increased LV fibrosis, cardiomyocyte hypertrophy, elevated NT-proBNP plasma levels, fluid and protein loss in pulmonary interstitium, impaired lung expansion, and alveolar-capillary membrane thickening. We report for the first time in HFpEF perivascular fluid cuff formation around extra-alveolar vessels with decreased respiratory compliance. Ultimately, these cardiopulmonary abnormalities resulted in impaired oxygenation. Our findings support the idea that this model can be used for testing novel therapeutic strategies to treat the ever growing HFpEF population.

Changes in overall ventricular myocardial architecture in the setting of a porcine animal model of right ventricular dilation.

Chronic pulmonary regurgitation often leads to myocardial dysfunction and heart failure. It is not fully known why secondary hypertrophy cannot fully protect against the increase in wall stress brought about by the increased end-diastolic volume in ventricular dilation. It has been assumed that mural architecture is not deranged in this situation, but we hypothesised that there might be a change in the pattern of orientation of the aggregations of cardiomyocytes, which would contribute to contractile impairment.

Biomarkers of cardiovascular stress and fibrosis in preclinical hypertrophic cardiomyopathy.

Sarcomeric gene mutation carriers without overt left ventricular hypertrophy (G+/LVH-) can harbour subclinical changes in cardiovascular structure and function that precede the development of hypertrophic cardiomyopathy (HCM). We sought to investigate if circulating biomarkers of cardiovascular stress and collagen metabolism among G+/LVH- individuals, measured at rest and following exercise provocation, yield further insights into the underlying biology of HCM.

The relationship of all-cause mortality to average on-treatment systolic blood pressure is significantly related to baseline systolic blood pressure: implications for interpretation of the Systolic Blood Pressure Intervention Trial study.

The SPRINT study demonstrated that targeting systolic blood pressure (SBP) less than 120 mmHg was associated with lower cardiovascular event and mortality rates. In the LIFE study, however, a lower achieved SBP was associated with increased mortality. Mean baseline SBP in SPRINT was 140 mmHg and a third of the population had a baseline SBP 132 mmHg or less, raising the question of whether the lower baseline SBP in SPRINT could in part account for these differences.

Hypertrophied myocardium is vulnerable to ischemia reperfusion injury and refractory to rapamycin-induced protection due to increased oxidative/nitrative stress.

Left ventricular hypertrophy (LVH) is causally related to increased morbidity and mortality following acute myocardial infarction (AMI) via still unknown mechanisms. Although rapamycin exerts cardioprotective effects against myocardial ischemia/reperfusion (MI/R) injury in normal animals, whether rapamycin-elicited cardioprotection are altered in the presence of LVH has yet to be determined. Pressure overload-induced cardiac hypertrophied mice and sham-operated controls were exposed to AMI by coronary artery ligation, and treated with vehicle or rapamycin  10 min before reperfusion. Rapamycin produced marked cardioprotection in normal control mice, whereas pressure overload-induced cardiac hypertrophied mice manifested enhanced myocardial injury, and was refractory to rapamycin-elicited cardioprotection evidenced by augmented infarct size, aggravated cardiomyocytes apoptosis, and worsening cardiac function. Rapamycin alleviated MI/R injury via ERK-dependent antioxidative pathways in normal mice, whereas cardiac hypertrophied mice manifested markedly exacerbated oxidative/nitrative stress after MI/R evidenced by the increased iNOS/gp91phox expression, superoxide production, total NO metabolites and nitrotyrosine content. Moreover, scavenging superoxide or peroxynitrite by selective gp91phox assembly inhibitor gp91ds-tat or ONOO- scavenger EUK134 markedly ameliorated MI/R injury, as shown by reduced myocardial oxidative/nitrative stress, alleviated myocardial infarction, hindered cardiomyocytes apoptosis, and improved cardiac function in aortic-banded mice. However, no additional cardioprotective effects was achieved when we combined rapamycin and gp91ds-tat or EUK134 in ischemic reperfused hearts with or without LVH. These results suggest that cardiac hypertrophy attenuated rapamycin-induced cardioprotection by increasing oxidative/nitrative stress and scavenging superoxide/peroxynitrite protects the hypertrophied heart from MI/R.

Endothelial Nitric Oxide Synthase-Induced Hypertrophy and Vascular Dysfunction Contribute to the Left Ventricular Dysfunction in Caveolin-1-/- Mice.

Caveolin-1 (Cav1)-/- mice display impaired development of left ventricular pressure and increased left ventricular wall thickness but no dilated ventricle; these are typical findings in patients with heart failure with preserved ejection fraction (HfpEF). Aiming to clarify if dysfunctional endothelial nitric oxide synthase (eNOS) influences cardiomyocyte contractility, cardiac conduction system, or afterload/vascular resistance, we studied Cav1-/-/eNOS-/- mice.

Electrocardiographic Markers of Sudden Cardiac Death (Including Left Ventricular Hypertrophy).

Although the electrocardiograph (ECG) was invented more than 100 years ago, it remains the most commonly used test in clinical medicine. It is easy to perform, relatively cheap, and results are readily available. Interpretation, however, needs expertise and knowledge. New data, phenomenon, and syndromes are continually discovered by the ECG. It is important to differentiate between normal and abnormal ECGs first and then try to correlate the findings with clinical pathologies. Furthermore, the ECG is an integral part of the screening model for a variety of conditions such as channelopathies, athletes, preoperative risk profile, and remains the cardiologist's best friend.