Rationale and design of the cardiovascular status in patients with endogenous cortisol excess study (CV-CORT-EX): a prospective non-interventional follow-up study.

BACKGROUND: Endogenous Cushing's syndrome (CS) results in increased cardiovascular (CV) morbidity and mortality. So far, most studies focussed on distinct disease entities rather than the integrity of the CV system. We here describe the design of the Cardiovascular Status in Endogenous Cortisol Excess Study (CV-CORT-EX), a study aiming to comprehensively investigate the health status of patients with endogenous CS (with a particular focus on CV phenotypes, biochemical aspects, quality of life, and psychosocial status). METHOD: A prospective non-interventional cohort study performed at a German tertiary referral centre. At the time of enrolment, patients will be categorised as: (1) newly diagnosed overt CS, (2) recurrent overt CS, (3) CS in remission, (4) presence of mild autonomous cortisol excess (MACE). The target cohorts will be n = 40 (groups 1 + 2), n = 80 (group 3), and n = 20 (group 4). Patients with overt CS at the time of enrolment will be followed for 12 months after remission (with re-evaluations after 6 and 12 months). At each visit, patients will undergo transthoracic echocardiography, cardiac magnetic resonance imaging, 24-h electrocardiogram, 24-h blood pressure measurement, and indirect evaluation of endothelial function. Furthermore, a standardised clinical investigation, an extensive biochemical workup, and a detailed assessment of quality of life and psychosocial status will be applied. Study results (e.g. cardiac morphology and function according to transthoracic echocardiography and cardiac magnetic resonance imaging; e.g. prevalence of CV risk factors) from patients with CS will be compared with matched controls without CS derived from two German population-based studies. DISCUSSION: CV-CORT-EX is designed to provide a comprehensive overview of the health status of patients with endogenous CS, mainly focussing on CV aspects, and the holistic changes following remission. TRAIL REGISTRATION: ClinicalTrials.gov ( https://clinicaltrials.gov/ ) NCT03880513, registration date: 19 March 2019 (retrospectively registered). Protocol Date: 28 March 2014, Version 2.

Left ventricular hypertrophy diagnosed after a stroke: a case report.

BACKGROUND: Stroke is a recognized clinical course of hypertrophic cardiomyopathy. This interesting case showed notable difference on the electrocardiogram of a patient 4 months prior to suffering a stroke and 10 days after suffering a stroke. The pre-stroke electrocardiogram showed atrial fibrillation with a narrow QRS complex, while the post-stroke electrocardiogram showed marked left ventricular hypertrophy. Left ventricular hypertrophy was diagnosed using the Sokolow-Lyon indices. The development of left ventricular hypertrophy a few days after suffering a stroke has not previously been reported. CASE PRESENTATION: An 83-year-old white British woman with a background history of permanent atrial fibrillation, hypertension, and previous stroke attended the emergency department with a 2-day history of exertional dyspnea, and chest tightness. On examination, she had bibasal crepitations with a systolic murmur loudest at the apex. In-patient investigations include an electrocardiogram, blood tests, chest X-ray, contrast echocardiogram, coronary angiogram, and cardiovascular magnetic resonance imaging. An electrocardiogram showed atrial fibrillation, with inferolateral T wave inversion, and left ventricular hypertrophy. A chest X-ray showed features consistent with pulmonary edema. A contrast echocardiogram showed marked hypertrophy of the mid to apical left ventricle, appearance consistent with apical hypertrophic cardiomyopathy. Coronary angiography showed eccentric shelf-type plaque with non-flow-limiting stenosis in the left coronary artery main stem. Cardiovascular magnetic resonance imaging reported findings highly suggestive of apical hypertrophic cardiomyopathy. Our patient was treated and discharged on rivaroxaban, bisoprolol, and atorvastatin with a follow-up in the cardiomyopathy outpatient clinic. CONCLUSIONS: Electrocardiogram diagnosis of left ventricular hypertrophy led to the diagnosis of apical hypertrophic cardiomyopathy in this patient. Left ventricular hypertrophy was only evident a few days after our patient suffered a stroke. The underlying mechanisms responsible for this remain unclear. Furthermore, differential diagnosis of hypertrophic cardiomyopathy should be considered in people with electrocardiogram criteria for left ventricular hypertrophy. Cardiovascular magnetic resonance imaging is an important diagnostic tool in identifying causes of left ventricular hypertrophy. Family screening should be recommended in patients with new diagnosis of hypertrophic cardiomyopathy.

Effect of increased left ventricle mass on ischemia assessment in electrocardiographic signals: rabbit isolated heart study.

BACKGROUND: Detailed quantitative analysis of the effect of left ventricle (LV) hypertrophy on myocardial ischemia manifestation in ECG is still missing. The associations between both phenomena can be studied in animal models. In this study, rabbit isolated hearts with spontaneously increased LV mass were used to evaluate the effect of such LV alteration on ischemia detection criteria and performance. METHODS: Electrophysiological effects of increased LV mass were evaluated on sixteen New Zealand rabbit isolated hearts under non-ischemic and ischemic conditions by analysis of various electrogram (EG) parameters. To reveal hearts with increased LV mass, LV weight/heart weight ratio was proposed. Standard paired and unpaired statistical tests and receiver operating characteristics analysis were used to compare data derived from different groups of animals, monitor EG parameters during global ischemia and evaluate their ability to discriminate between unchanged and increased LV as well as non-ischemic and ischemic state. RESULTS: Successful evaluation of both increased LV mass and ischemia is lead-dependent. Particularly, maximal deviation of QRS and area under QRS associated with anterolateral heart wall respond significantly to even early phase (the 1st-3rd min) of ischemia. Besides ischemia, these parameters reflect increased LV mass as well (with sensitivity reaching approx. 80%). However, the sensitivity of the parameters to both phenomena may lead to misinterpretations, when inappropriate criteria for ischemia detection are selected. Particularly, use of cut-off-based criteria defined from control group for ischemia detection in hearts with increased LV mass may result in dramatic reduction (approx. 15%) of detection specificity due to increased number of false positives. Nevertheless, criteria adjusted to particular experimental group allow achieving ischemia detection sensitivity of 89-100% and specificity of 94-100%, respectively. CONCLUSIONS: It was shown that response of the heart to myocardial ischemia can be successfully evaluated only when taking into account heart-related factors (such as LV mass) and other methodological aspects (such as recording electrodes position, selected EG parameters, cut-off criteria, etc.). Results of this study might be helpful for developing new clinical diagnostic strategies in order to improve myocardial ischemia detection in patients with LV hypertrophy.

Cyclovirobuxinum D alleviates cardiac hypertrophy in hyperthyroid rats by preventing apoptosis of cardiac cells and inhibiting the p38 mitogen-activated protein kinase signaling pathway.

OBJECTIVE: To investigate the underlying mechanisms of cyclovirobuxinum D (Cvb-D) on alleviating cardiac hypertrophy in rats. METHODS: Sprague-Dawley rats were randomly divided into 5 groups: control group; levothyroxine-induced cardiac hypertrophy group (model); levothyroxine-induced cardiac hypertrophy + Cvb-D group (Cvb-D); levothyroxine-induced cardiac hypertrophy + captopril group (captopril); levothyroxine-induced cardiac hypertrophy + SB203580 group (SB203580), n=10 for each group. Rats were daily administered the respective drugs continuously for14 days by gastric gavage. A rat model of cardiac hypertrophy was established by intraperitoneal injection of levothyroxine to investigate whether Cvb-D protects against cardiac hypertrophy by inhibiting the p38 mitogen-activated protein kinase (MAPK) signaling pathway and preventing apoptosis of cardiac cells. RESULTS: Treatment with Cvb-D significantly deceased left ventricle hypertrophy, improved the histopathology, hemodynamic conditions, and cardiac function in rats with cardiac hypertrophy. Compared with the normal control group, in rats with cardiac hypertrophy, expression of bax in the heart and phospho-p38 MAPK protein levels were significantly up-regulated (P<0.01 or 0.05), whereas the bcl-2 protein level was down-regulated (P<0.01). In contrast, Cvb-D treatment reversed the changes in bax and phospho-p38 MAPK protein levels but increased the bcl-2 protein level (P<0.01 or 0.05), and these effects were similar to those of captopril and SB203580 (a specific p38MAPK inhibitor) treatment. Furthermore, both Cvb-D, captopril and SB203580 reduced mRNA expression of p38α, p38ß, c-fos, and c-jun mRNA, and Cvb-D had a stronger effect (P<0.01). CONCLUSION: These results demonstrate that Cvb-D protects against cardiac hypertrophy, which is possibly mediated by prevention of cardiac cell apoptosis and inhibition of the p38MAPK signaling pathway.

Dietary management of heart failure: room for improvement?

There is growing awareness of the role of diet in both health and disease management. Much data are available on the cardioprotective diet in the primary and secondary prevention of CVD. However, there is limited information on the role of diet in the management of heart failure (HF). Animal models of HF have provided interesting insight and potential mechanisms by which dietary manipulation may improve cardiac performance and delay the progression of the disease, and small-scale human studies have highlighted beneficial diet patterns. The aim of this review is to summarise the current data available on the role of diet in the management of human HF and to demonstrate that dietary manipulation needs to progress further than the simple recommendation of salt and fluid restriction.

Scar dechanneling: new method for scar-related left ventricular tachycardia substrate ablation.

BACKGROUND: Ventricular tachycardia (VT) substrate ablation usually requires extensive ablation. Scar dechanneling technique may limit the extent of ablation needed. METHODS AND RESULTS: The study included 101 consecutive patients with left ventricular scar-related VT (75 ischemic patients; left ventricular ejection fraction, 36 ± 13%). Procedural end point was the elimination of all identified conducting channels (CCs) by ablation at the CC entrance followed by abolition of residual inducible VTs. By itself, scar dechanneling rendered noninducibility in 54.5% of patients; ablation of residual inducible VT increased noninducibility to 78.2%. Patients needing only scar dechanneling had a shorter procedure (213 ± 64 versus 244 ± 71 minutes; P = 0.027), fewer radiofrequency applications (19 ± 11% versus 27 ± 18%; P = 0.01), and external cardioversion/defibrillation shocks (20% versus 65.2%; P < 0.001). At 2 years, patients needing scar dechanneling alone had better event-free survival (80% versus 62%) and lower mortality (5% versus 11%). Incomplete CC-electrogram elimination was the only independent predictor (hazard ratio, 2.54 [1.06-6.10]) for the primary end point. Higher end point-free survival rates were observed in patients noninducible after scar dechanneling (log-rank P = 0.013) and those with complete CC-electrogram elimination (log-rank P = 0.013). The complications rate was 6.9%, with no deaths. CONCLUSIONS: Scar dechanneling alone results in low recurrence and mortality rates in more than half of patients despite the limited ablation extent required. Residual inducible VT ablation improves acute results, but patients who require it have worse outcomes. Recurrences are mainly related to incomplete CC-electrogram elimination.

[MicroRNA and left ventricular hypertrophy].

MicroRNAs (miRNA) plays an important role in biological development and disease occurrence and development, and acts as a "main switch" in biology. Among patients of essential hypertension, around 1/3 would suffer left ventricular hypertrophy (LVH). Hence, essential hypertension becomes an independent risk factor for cardiovascular diseases. And miRNAs plays an important role in the occurrence and development of LVH. This paper reviewed the role of miRNA in regulating the stress signaling pathway, defined its impact on the occurrence of LVH, and further emphasized the opportunities and challenges of miRNA as a biomarker and therapeutic target.

Electrocardiographic imaging-based recognition of possible induced bundle branch blocks during transcatheter aortic valve implantations.

AIMS: Conventional electrocardiogram (ECG)-based diagnosis of left bundle branch block (LBBB) in patients with left ventricular hypertrophy (LVH) is ambiguous. Left ventricular hypertrophy is often seen in patients with severe aortic stenosis in which a transcatheter aortic valve implantation (TAVI) frequently results in a LBBB due to the mechanical interaction of the artificial valve and the conduction system. In this feasibility study, we propose and evaluate the sensitivity of a new electrocardiographic imaging tool; the cardiac isochrone positioning system (CIPS), visualizing the cardiac activation to detect interventricular conduction patterns pre- and post-TAVI. METHODS AND RESULTS: The CIPS translates standard 12-lead ECG into ventricular isochrones, representing the activation sequence. It requires a patient-specific model integrating heart, lungs, and other thoracic structures derived from multi-slice computed tomography. The fastest route-based algorithm was used to estimate the activation isochrones and the results were compared with standard ECG analysis. In 10 patients the CIPS was used to analyse 20 ECGs, 10 pre- and 10 post-TAVI. In 11 cases the CIPS results were in agreement with the ECG-based diagnosis. In two cases there was partial agreement and in seven cases there was disagreement. In four of these cases, the clinical history of the patients favoured interpretation as assessed by CIPS, for the remaining three, it is unknown which method correctly classified the activation. CONCLUSION: This feasibility study applying the CIPS shows promising results to classify conduction disorders originating from the left anterior or posterior ventricular wall, or the septum. The visualization of the activation isochrones as well as ventricular model-derived features might support TAVI procedures and the therapy selection afterwards.

Acute caffeine poisoning resulting in atrial fibrillation after guarana extract overdose.

UNLABELLED: Guarana (Paullinia cupana) is the climbing vine native to Amazon Basin, characterized by high caffeine content in its seeds. Guarana extract is a common ingredient of energy drinks used in order to boost energy and physical endurance and increase alertness. Severe caffeine intoxication is rare, but may be life-threatening mostly due to supraventricular and ventricular dysrhythmias. OBJECTIVES: We present the case of intentional caffeine poisoning after ingestion of tablets containing guarana extract, complicated by atrial fibrillation. CASE REPORT: A44-year-old man with no significant medical history was admitted to hospital about 21 h after ingestion of guarana extract containing 1.6 g of caffeine. Typical symptoms of caffeine toxicity, i.e. nausea, vomiting, anxiety and palpitaions, occurred shortly after ingestion. On admission, he was conscious, with blood pressure of 136/86 mmHg, heart rate of 106-113 beats per minute, fever of 37.8 °C, and symmetrically increased deep tendon reflexes. QTc interval in electrocardiogram was prolonged to 0.542 s. Laboratory tests revealed hypokalemia, hyperglycemia, leukocytosis, as well as elevated creatinine and creatine phosphokinase levels. Approximately 45 h post ingestion, the patient developed atrial fibrillation with fast ventricular rhythm. Tachydysrythmia subsided after infusion of amiodarone and restoration of electrolyte balance. Echocardiogram revealed presence of asymmetrical hypertrophy of the left ventricle with the systolic anterior motion of the mitral valve and normal left ventricular outflow tract gradient suggesting non-obstructive hypertrophic cardiomyopathy. CONCLUSION: Acute caffeine poisoning may result in atrial fibrillation, especially in predisposed patients with underlying hypertrophic cardiomyopathy.

Effects of Roselle on arterial pulse pressure and left ventricular hypertrophy in hypertensive patients.

OBJECTIVE: To characterize the effects of regular Roselle ingestion on blood pressure and left ventricular hypertrophy (LVH) in patients with established moderate essential hypertension. METHODS: This non-randomized quasi-experimental study was conducted in Kafr El-Shaikh, Egypt, for 8 weeks, from September 2012 to November 2012. The effects of a 4-week period of regular Roselle ingestion followed by a 4-week recovery period on systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and heart rates (HR) was studied in 2 equal, gender- and age-matched groups (n=50 each; average age - 50+/-5 years) of normotensive subjects, and patients with moderate essential hypertension. Electrocardiographic assessments of LVH were also made prior to, and at the end of both treatment and recovery periods. RESULTS: Pulse pressure (PP) significantly fell from baseline values by 10.9% (normotensive group [NG]), 21.2% (hypertensive group [HG]); SBP by 10% (NG), 19.6% (HG); DBP by 9.5% (NG), 18.7% (HG), and HR by 14.6% (NG), 17.1% (HG) by the end of week 4 of treatment. Following treatment cessation, SBP, DBP, PP, and HR returned to pretreatment levels over 4 weeks. Before intervention, none of the normotensive subjects, but 14 hypertensive patients showed LVH. However, Roselle treatment was associated with regression of LVH in 10 patients with only 4 patients showing LVH after 4 weeks of treatment. This became 10 patients 4 weeks after ceasing treatment. CONCLUSION: These findings empirically suggest favorable cardiovascular effects of Roselle in patients with established moderate essential hypertension.

Allopurinol reduces left ventricular mass in patients with type 2 diabetes and left ventricular hypertrophy.

OBJECTIVES: This study sought to ascertain whether high-dose allopurinol causes regression of left ventricular mass (LVM) in patients with type 2 diabetes mellitus (T2DM). BACKGROUND: Left ventricular hypertrophy (LVH) is common in T2DM and contributes to patients' high cardiovascular (CV) event rate. Oxidative stress (OS) has been implicated in LVH development, and allopurinol has been previously shown to reduce vascular OS. We therefore investigated whether allopurinol causes regression of LVH in patients with T2DM. METHODS: We conducted a randomized, double-blind, placebo-controlled study of 66 optimally-treated T2DM patients with echocardiographic evidence of LVH. Allopurinol, 600 mg/day, or placebo was given over the study period of 9 months. The primary outcome was reduction in LVM as calculated by cardiac magnetic resonance imaging at baseline and at 9 months' follow-up. Secondary endpoints were change in flow-mediated dilation and augmentation index. RESULTS: Allopurinol significantly reduced absolute LVM (-2.65 ± 5.91 g vs. placebo group +1.21 ± 5.10 g [p = 0.012]) and LVM indexed to body surface area (-1.32 ± 2.84 g/m(2) vs. placebo group +0.65 ± 3.07 g/m(2) [p = 0.017]). No significant changes were seen in either flow-mediated dilation or augmentation index. CONCLUSIONS: Allopurinol causes regression of LVM in patients with T2DM and LVH. Regression of LVH has been shown previously to improve CV mortality and morbidity. Therefore, allopurinol therapy may become useful to reduce CV events in T2DM patients with LVH. (Allopurinol in Patients with Diabetes and LVH; UKCRN 8766).

Organic nitrates favor regression of left ventricular hypertrophy in hypertensive patients on chronic peritoneal dialysis.

The aim of the study was to evaluate the effect of nitrates on left ventricular hypertrophy (LVH) in hypertensive patients on chronic peritoneal dialysis (PD). Sixty-four PD patients with hypertension were enrolled in this study. All patients accepted antihypertensive drugs at baseline. Thirty-two patients (nitrate group) took isosorbide mononitrate for 24 weeks. The remaining 32 patients (non-nitrate group) took other antihypertensive drugs. Blood pressure (BP), left ventricular mass index (LVMI) and plasma asymmetric dimethylarginine (ADMA) were monitored. Subjects with normal renal function were included as the control group (n = 30). At baseline, plasma ADMA levels in PD patients were significantly higher than the control group, but there was no significant difference in plasma ADMA levels between the two groups. At the end of the 24-week period, BP, LVMI, LVH prevalence and plasma ADMA levels in the nitrate group were significantly lower than those in the non-nitrate group. BP did not show a significant difference between 12 and 24 weeks in the nitrate group with a reduced need for other medication. Logistic regression analysis showed that nitrate supplementation and SBP reduction were independent risk factors of LVMI change in PD patients after adjusting for age, gender, diabetes history and CCB supplementation. It was concluded that organic nitrates favor regression of LVH in hypertensive patients on chronic peritoneal dialysis, and nitrates may be considered for use before employing the five other antihypertensive agents other than nitrates.

In vivo suppression of microRNA-24 prevents the transition toward decompensated hypertrophy in aortic-constricted mice.

RATIONALE: During the transition from compensated hypertrophy to heart failure, the signaling between L-type Ca(2+) channels in the cell membrane/T-tubules and ryanodine receptors in the sarcoplasmic reticulum becomes defective, partially because of the decreased expression of a T-tubule-sarcoplasmic reticulum anchoring protein, junctophilin-2. MicroRNA (miR)-24, a junctophilin-2 suppressing miR, is upregulated in hypertrophied and failing cardiomyocytes. OBJECTIVE: To test whether miR-24 suppression can protect the structural and functional integrity of L-type Ca(2+) channel-ryanodine receptor signaling in hypertrophied cardiomyocytes. METHODS AND RESULTS: In vivo silencing of miR-24 by a specific antagomir in an aorta-constricted mouse model effectively prevented the degradation of heart contraction, but not ventricular hypertrophy. Electrophysiology and confocal imaging studies showed that antagomir treatment prevented the decreases in L-type Ca(2+) channel-ryanodine receptor signaling fidelity/efficiency and whole-cell Ca(2+) transients. Further studies showed that antagomir treatment stabilized junctophilin-2 expression and protected the ultrastructure of T-tubule-sarcoplasmic reticulum junctions from disruption. CONCLUSIONS: MiR-24 suppression prevented the transition from compensated hypertrophy to decompensated hypertrophy, providing a potential strategy for early treatment against heart failure.

Prevalence and progression of cardiovascular calcifications in peritoneal dialysis patients: A prospective study.

BACKGROUND: Patients on dialysis may have abnormal serum levels of Ca, P and parathyroid hormone, with related bone diseases. This population has an increased risk of death, with cardiovascular calcification (CC) a contributing factor. Patients on peritoneal dialysis appear to be at increased risk of hyperlipidemia, a contributing factor to atherosclerotic plaque formation. Although several studies have described the presence and progression of CC in hemodialysis populations, there are fewer data in patients on peritoneal dialysis. STUDY DESIGN: The Renal Osteodystrophy and Calcifications: Key factors in Peritoneal Dialysis (ROCK-PD) study was a 36-month, prospective observational study conducted in Italy. The study examined the presence and progression of CC in two cardiac valves and five arterial sites. The potential associations of serum Ca and P with mortality and cardiovascular morbidity, demographic, clinical and blood chemistry variables was investigated. RESULTS: CC was present in 77% of patients at baseline (N=369) and in 90% of patients by study end (N=145), progressing in 73% of patients. There were 42 deaths (11%). Analyses showed a marked correlation between baseline P levels and the presence of left ventricular hypertrophy. However, there were no consistent correlations between serum Ca or P with mortality or morbidity. CONCLUSIONS: CC was common in peritoneal dialysis patients and progressed in a majority of patients.

T-wave alternans and left ventricular wall thickness in predicting arrhythmic risk in patients with hypertrophic cardiomyopathy.

BACKGROUND: Regional heterogeneity of left ventricular (LV) hypertrophy may contribute to arrhythmic vulnerability in patients with hypertrophic cardiomyopathy (HCM). The aim of the present study was to investigate the relationship between LV wall thickness (LVWT) and microvolt T-wave alternans (TWA), a surrogate risk marker of ventricular tachyarrhythmias (VTAs). METHODS AND RESULTS: A total of 157 consecutive HCM patients underwent 2-D echocardiography and TWA-exercise testing, and assessment of arrhythmic burden in a follow up of a median 3.7 years. VTAs were commoner in the non-negative groups (NN-TWA: n=72, TWA+ and indeterminate outcome; 29 events, P<0.02; TWA+: n=34; 14 events, P=0.01), than in the negative TWA group (n=85, 16 events). TWA+ patients were older (P<0.04) and had greater maximal LVWT and LV mass (P=0.02 and P=0.05, respectively), whereas NN-TWA linked only with increased LV mass (P=0.05). Regionally, the TWA+ group had greater inferior LVWT (P<0.05). TWA+ outcome positively correlated with maximal LVWT (r=0.2, P=0.05), and basal/equatorial/apical inferior LVWT (BA6: r=0.2, P=0.05 and EQ6: r=0.2 P=0.03, AP6: r=0.2, P=0.04). Multivariate analysis identified left atrium size, max LVWT and EQ6 with predictive association for TWA+ outcome. CONCLUSIONS: Positive and NN-TWA outcomes are associated with increased LV mass. Moreover, TWA+ is associated with maximal and regional LVWT in HCM patients at risk of arrhythmic events. The present findings support the complementary role of key regional LVWTs in a risk stratification model.

Cardiac mortality in {beta}-thalassemia major: resting but not dobutamine stress echocardiography predicts mortality among initially cardiac disease-free patients in a prospective 12-year study.

AIMS: Cardiac death remains the principal cause of mortality in beta-thalassemia major (beta-TM). Echocardiography may provide additional information, incremental to haematological profile, both for guiding chelation therapy and to assess prognosis. METHODS AND RESULTS: Between 1993 and 1995, 36 patients with beta-TM and normal cardiac function and 25 normal volunteers underwent evaluation using resting and dobutamine stress echocardiography (DSE). Dobutamine stress echocardiography was performed at baseline and repeated after 2 years. The primary endpoint was cardiac mortality. During a 12-year observation period, seven patients (19%) died from heart failure. All seven deaths occurred among the cohort of 12 patients with median ferritin concentrations >or= 2800 ng/mg. In addition, a resting left ventricular ejection fraction (LVEF) < 60% was also associated with increased late mortality. In multivariate analysis, increased serum ferritin levels and reduced LVEF but not DSE or other haematological variables were independent survival determinants. CONCLUSION: Resting LVEF provides prognostic information that is additional to ferritin levels among patients with beta-TM.

L-carnitine supplementation decreases the left ventricular mass in patients undergoing hemodialysis.

BACKGROUND: Patients on long-term hemodialysis become deficient in carnitine and are frequently treated with carnitine supplementation to offset their renal anemia, lipid abnormality and cardiac dysfunction. The therapeutic value of carnitine supplementation on left ventricular hypertrophy (LVH) in patients with normal cardiac systolic function remains uncertain. METHODS AND RESULTS: The cardiac morphology and function of 10 patients given 10 mg/kg of L-carnitine orally, immediately after hemodialysis sessions 3 times per week for a 12-month period were compared with 10 untreated control patients. Using echocardiography, left ventricular fractional shortening (LVFS) and left ventricular mass index (LVMI) were measured before and after the study period. As a result, amounts of serum-free carnitine increased from 28.4+/-4.7 to 58.5+/-12.1 micromol/L. The LVMI decreased significantly from 151.8+/-21.2 to 134.0+/-16.0 g/m(2) in treated patients (p<0.01), yet the LVMI in untreated control patients did not change significantly (ie, from 153.3+/-28.2 to 167.1+/-43.1 g/m(2)). However, LVFS values remained unchanged in both groups. Although L-carnitine promoted a 31% reduction in erythropoietin requirements, hematocrit and blood pressure did not change during the study period. CONCLUSIONS: Supplementation with L-carnitine induced regression of LVH in patients on hemodialysis, even for those with normal systolic function.

Effects of yixin jiangya capsules on insulin resistance and timor necrosis factor-alpha in cases of primary hypertension with left ventricular hypertrophy.

OBJECTIVES: To observe the effects of yixin jiangya Capsules ([Chinese characters: see text] capsules for nourishing the heart and lowering blood pressure) on insulin resistance (IR) and tumor necrosis factor-alpha (TNF-alpha) in patients with primary hypertension with left ventricular hypertrophy (LVH). METHODS: Totally 93 cases were randomly divided into a control group of 31 cases taking Enalapril and a treatment group of 62 cases taking Enalapril and yixin jiangya Capsules. RESULTS: Fasting serum insulin (FSI) and TNF-alpha obviously increased and insulin sensitive index (ISI) significantly decreased in both groups before treatment as compared to those of a healthy group. After treatment, FSI, TNF-alpha and fasting blood glucose (FBG) obviously decreased and ISI remarkably increased in the treatment group, while ISI significantly increased and TNF-alpha obviously decreased in the control group. The curative effect in the treatment group was remarkably superior to that in the control group. FSI was positively related to TNF-a before treatment in both groups. CONCLUSION: FSI and TNF-alpha obviously increase and ISI significantly decreases in patients with primary hypertension with LVH. FSI and TNF-alpha influencing each other are involved in the generation and development of hypertension. Yixin jiangya Capsules can improve IR and decrease TNF-alpha.