Evidence Of Left Ventricular Hypertrophy Research Articles

Left ventricular hypertrophy is a possible biomarker for early mortality after type B aortic dissection

ObjectiveData regarding the cardiac abnormalities associated with Stanford type B aortic dissection (TBAD) and whether these abnormalities are related to outcomes are limited. We describe the prevalence of cardiac abnormalities in patients with TBAD as detected by echocardiography. MethodsThis retrospective review included patients with TBAD presenting between 1990 and 2016. Echocardiograms performed within 6 weeks of acute TBAD were reviewed. Cardiac function, valve abnormalities, and stigmata of hypertensive heart disease including left ventricular hypertrophy (LVH) were ascertained. Characteristics of patients who did and did not receive echocardiograms were compared. Outcomes of patients with and without evidence of LVH on echocardiography were also compared. ResultsOf 239 patients with TBAD, 90 had echocardiograms performed within 6 weeks of acute TBAD (74% male; mean age, 57.8 ± 13.2 years). Echocardiograms were obtained at a median of 2 days (range, 0-41 days) from acute TBAD. Patients who had echocardiograms were more likely to present with malperfusion (28% vs 14%; P < .01) and had a trend toward increased operative repair during the subacute phase (17.4% vs 9.5%; P = .07) compared with patients who did not receive an echocardiogram. A majority of patients (57%) had at least mild LVH, including 39% of patients without a prior diagnosis of hypertension. Fibrocalcific changes associated with hypertension, including aortic sclerosis and mitral annular calcification, were noted in 40% and 11% of the patients, respectively. Among patients with LVH, there was a trend toward higher all-cause mortality (35% vs 23%; P = .21) and a younger age at death (58 ± 14 years vs 66 ± 13 years; P = .19) despite a similar age at TBAD onset. In a multivariable analysis controlling for age, sex, and admission estimated glomerular filtration rate, LVH independently predicted all-cause mortality (hazard ratio, 2.38; 95% confidence interval, 1.02-5.56; P = .04). ConclusionsLVH and other findings of hypertensive heart disease are common in patients with TBAD. LVH predicted all-cause mortality after TBAD in this small group of patients. Further exploration of the relationship between the chronic effects of hypertension and using LVH as an objective biomarker to risk stratify patients with TBAD and long-term outcomes after TBAD is warranted.

Association between potassium levels and mortality risk in hypertensive patients with or without electrocardiographic left ventricular hypertrophy

Introduction: Knowledge on optimal potassium levels in relation to hypertension with evidence of left ventricular hypertrophy (LVH) remains limited. Therefore, we investigated the association and i...

Galectin‑3 in patients with left ventricular hypertrophy and metabolic syndrome

Objective. To investigate the serum levels of galectin‑3 in patients with metabolic syndrome (MS) and in patients with combination of MS and left ventricular hypertrophy (LVH), as well as to define the role of this marker of fibrosis in MS.Design and methods. The study included 43 patients with MS (33 patients had LVH), and 33 patients of comparable age without MS (LVH was diagnosed in 10). The level of serum galectin‑3 was determined by enzyme immunoassay kits Platinum ELISA.Results. The average level of galectin‑3 in the MS group was significantly higher (1,89 ± 1,71 ng/ml), compared to the group without MS (1,03 ± 0,22 ng/ml, p = 0,006). The study showed a positive correlation between the level of galectin‑3 and LVH (r = 0,323, p = 0,004). The mean value of galectin‑3 in patients with no evidence of LVH was 1,2 ± 0,76 ng/ml, in patients with LVH — 2,1 ± 2,02 ng/ml.Conclusions. In patients with MS the level of galectin‑3 was higher than in patients without MS, and in patients with MS and concomitant LVH it was higher than in patients without LVH. In patients with MS and LVH increased galectin‑3 levels may indicate the severity of myocardial fibrosis and help for prognosis evaluation.

Contemporary Septal Reduction Therapy in Drug-Refractory Hypertrophic Obstructive Cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is a complex and relatively common genetic cardiac disease that has been the subject of intense investigation for over 50 years. Most patients with HCM are asymptomatic, but some develop symptoms, often many years after the appearance of electrocardiographic or echocardiographic evidence of left ventricular hypertrophy. Symptoms due to the left ventricular outflow tract obstruction frequently worsen over time, requiring septal reduction therapy (SRT) despite optimal medical therapy. Percutaneous transluminal septal myocardial ablation (PTSMA) and surgical myectomy are collectively known as SRT. In this review, we will focus on the emerging concept and practical implication of SRT and the available evidence on either PTSMA or surgical myectomy in the literature.

Echocardiographic changes with non-invasive ventilation and CPAP in obesity hypoventilation syndrome

RationaleDespite a significant association between obesity hypoventilation syndrome (OHS) and cardiac dysfunction, no randomised trials have assessed the impact of non-invasive ventilation (NIV) or CPAP on cardiac structure and function...

A Comparative Study of Electrocardiographic and Echocardiographic Evidence of Left ventricular Hypertrophy

A Comparative Study of Electrocardiographic and Echocardiographic Evidence of Left ventricular Hypertrophy

Unusual Presentation of Atypical Infantile Pompe Disease in the Newborn Period with Left Ventricular Hypertrophy

Pompe disease, also known as glycogen storage disease Type II, is a lysosomal storage disorder caused by α-glucosidase deficiency. In general, the clinical spectrum varies with respect to the age of onset, residual enzyme activity and organ involvement. Infantile onset disease has two subtypes: classical and non-classical (atypical). This case report describes the case of a newborn who presented with generalized hypotonia and elevated serum enzyme levels of aspartate aminotransferase 93 IU/L, lactate dehydrogenase 888 IU/L and creatine kinase 670 μg/L. The electrocardiogram showed short PR interval with large QRS complexes with echocardiography suggesting evidence of left ventricular hypertrophy with infiltration in its walls. On the basis of the clinical signs and laboratory results, dried blood spots from the baby were tested to determine the acid α-glucosidase (GAA) activity, and the result confirmed that the GAA activity was only 1.42 units, normal range 5.5 to 29.6 units, leading to a diagnosis of Pompe disease (atypical infantile). Recognizing this disease and initiating enzyme replacement therapy in infants at the earliest can improve the quality of life of patients.

Evaluation and management of patients referred to a tertiary-level hypertension clinic in Cape Town, South Africa.

Hypertension remains a global health burden, with a high incidence of long-term morbidity and mortality. To evaluate blood pressure (BP) control, factors associated with poor BP control, target organ damage (TOD), white-coat hypertension, treatment-resistant hypertension and secondary hypertension in patients referred to a tertiary-level hypertension clinic. This was a prospective case-control study of patients referred for specialist hypertension management. Patient parameters recorded included age, gender, body mass index, uric acid, cholesterol, screening BP, follow-up BP, TOD and medications. We also recorded causes of secondary hypertension. Net BP change and the percentage achieving target BP were calculated in all patients followed up. A total of 175 patients were sampled (72 males and 103 females, mean age 46.5 years). Of the patients 16.6% had a normal screening BP; 62.9% of patients were followed up, and 43.6% of these achieved BP control. After intervention, there was a net drop of 13.2 mmHg (range 7.9 - 18.4) in systolic BP and of 3.8 mmHg (4.4 - 12.0) in diastolic BP. Of all the patients, 12.6% had resistant hypertension, 49.1% had evidence of left ventricular hypertrophy and 18.3% had microalbuminuria; 13.1% of the patients were diagnosed with secondary hypertension. Specialist intervention was useful in identifying patients with white-coat and secondary hypertension, as well as in improving hypertension control in patients with apparent treatment-resistant hypertension. However, a significant percentage of patients did not reach target BP, and further efforts are required to identify the underlying causes for this.

Association of Traditional Cardiovascular Risk Factors With Development of Major and Minor Electrocardiographic Abnormalities: A Systematic Review.

Electrocardiographic (ECG) abnormalities are prevalent in middle aged and are associated with risk of adverse cardiovascular events. It is unclear whether and to what extent traditional risk factors are associated with the development of ECG abnormalities. To determine whether traditional cardiovascular risk factors are associated with the presence or development of ECG abnormalities, we performed a systematic review of the English-language literature for cross-sectional and prospective studies examining associations between traditional cardiovascular risk factors and ECG abnormalities, including major and minor ECG abnormalities, isolated nonspecific ST-segment and T-wave abnormalities, other ST-segment and T-wave abnormalities, QT interval, Q waves, and QRS duration. Of the 202 papers initially identified, 19 were eligible for inclusion. We examined data analyzing risk factor associations with ECG abnormalities in individuals free of cardiovascular disease. For composite major or minor ECG abnormalities, black race, older age, higher blood pressure, use of antihypertensive medications, higher body mass index, diabetes, smoking, and evidence of left ventricular hypertrophy or higher left ventricular mass are the factors most commonly associated with prevalence and incidence. Risk factor associations differ somewhat according to types of specific ECG abnormalities. Because major and minor ECG abnormalities have important and independent prognostic significance, understanding the groups at risk for their development may inform prevention strategies focused on modifiable risk factors to reduce the burden of ECG abnormalities, which may in turn promote CVD prevention.

Prevalence of Cardiovascular Disorders Among Iranian Elite Athletes.

BackgroundAthletes’ health is an important issue and for promoting it, pre-participation examination (PPE) is widely performed by responsible bodies around the world.ObjectivesThis study was to determine prevalence of cardiovascular disorders among athletes participating in the Asian games and answering the question whether the electrocardiogram (ECG) is a necessary part of pre-participation examination (PPE) for prevention of sudden cardiac death.Materials and MethodsAll athletes participated at Asian games came to sports medicine federation for a PPE including a comprehensive questionnaire, physical examination and ECG. In this retrospective study all profiles of 338 athletes have been studied as well as their electrocardiograms. Multiple logistic regressions as well as Firth’s bias reduction were used with R statistical software and SPSS. For predicting the changes in ECG, receiver operating characteristic (ROC) curve has done.ResultsAmong 388 athletes, 80 (20.6%) were female and 308 (79.4%) male with mean age of 23.2 + 8 years. Nine athletes (2.3%) were smokers, 28 of them (7.2%) experienced chest pain and discomfort, 45 of them (13.3%) had palpitations and 28 (7.2%) had history of anemia. Study of their electrocardiograms showed that long Q-T interval was not seen for anyone, but evidence of left ventricular hypertrophy was seen in 12 (3.1%), inverted T wave in 6 (1.5%), and right bundle branch block in 45 (13.3%).ConclusionsPPE provides very important information of athletes’ health. This study has shown that there was not any significant relation between current examination and electrocardiogram changes but regarding the ECG changes we recommend it as a routine part of PPE.

Abstract 48: Long-term Effects of an Intensive Lifestyle Intervention on Electrocardiographic Evidence of Left Ventricular Hypertrophy: The Action for Health in Diabetes (Look AHEAD) Trial

Introduction: Left ventricular hypertrophy assessed by electrocardiography (ECG-LVH) is a marker of subclinical cardiac damage and a strong predictor of cardiovascular events. The prevalence of ECG-LVH is increased in obesity and type 2 diabetes; thus, exercise and weight loss are recommended to lower cardiovascular disease (CVD) risk in these individuals. However, there are no data on the long term effects of diet- and/or exercise-induced weight loss on ECG-LVH. Hypothesis: We hypothesized that an intensive lifestyle intervention targeting weight loss through caloric restriction and increased physical activity reduces the incidence of ECG-LVH in overweight and obese adults with type 2 diabetes. Methods: We included 4,549 Look AHEAD participants without ECG-LVH at baseline who were randomized to a 10-year lifestyle intervention (ILI, n=2,287) or diabetes support and education (DSE, n=2,262) (mean age = 58.7±6.8 years, 64.5% White). ECG-LVH defined by the Cornell voltage criteria (RaVL + SV3 &gt;2800 μV in men and &gt;2000 μV in women) was assessed every 2 years. Proportional hazards regression was used to compare the incidence of ECG-LVH (defined as time to first occurrence) and mixed models were used to compare changes in absolute Cornell voltage over time between intervention groups, with tests of interactions by gender, race/ethnicity and baseline CVD status. Analyses were performed according to the intention-to-treat principle and all available follow-up data were included. Results: Baseline characteristics were similar between intervention groups, except for lower systolic blood pressure in the ILI vs. DSE group: mean (SE) = 127.6 (0.4) mmHg vs. 129.0 (0.4) mmHg, respectively (p=0.007). Over a median 9.5 years of follow-up, there were 162 cases of incident ECG-LVH in the ILI group (7.1%) and 181 cases in the DSE group (8.0%): HR=0.89, 95% CI=0.71-1.09, p=0.24. Intervention group interactions were not significant for prior CVD (p=0.53) or gender (p=0.74), but were of borderline significance for race/ethnicity (p=0.058). Among African Americans, ILI was estimated to be protective relative to DSE (HR=0.59, 95% CI= 0.38-0.91); there was no significant interaction for other race/ethnicity groups. Similar results were found after multivariate adjustment. In the mixed model analysis, the mean (SE) Cornell voltage was slightly lower in the ILI group compared to the DSE group after adjusting for the baseline value, age, gender, race/ethnicity, and prior CVD: 1369.2 (5.4) μV vs. 1381.9 (5.4) μV, respectively (p=0.07). Accounting for changes in blood pressure and anti-hypertensive medication use did not alter the results. Conclusions: A long-term intensive lifestyle intervention in overweight and obese adults with type 2 diabetes does not significantly lower overall incident ECG-LVH. The protective effect observed in African Americans, however, warrants further investigation.

Abstract 237: Prognostic Significance of Left Ventricular Hypertrophy (lvh) by Electrocardiography in a Minority-predominant Heart Failure (hf) Cohort

Background: Left ventricular Hypertrophy (LVH) has been associated with higher cardiovascular morbidity and mortality but most of these studies were conducted in majority (white) populations. LVH is known to be more common in African Americans (AA) who also have a higher prevalence of cardiovascular morbidity and mortality. The prognostic significance of LVH in AA with Heart Failure (HF) has not been well studied. Methods: We performed a retrospective analysis of a predominantly minority HF cohort (69.3% AA); after obtaining approval from our institutional review board. Our primary goal was to compare the HF outcomes [All-cause hospitalizations (ACH), hospitalizations primarily due to HF and ER visits] in patients with EKG evidence of LVH versus those without LVH. We also examined the racial (Blacks vs Whites), gender (males vs females) and age-based (≥60 Vs &lt;60 years) differential impact of LVH on HF outcomes and determined the prevalence of LVH in the cohort. Levene’s Test and t-test were used to analyze the data for equality of variances and means respectively. Result: Our HF cohort consisted of 599 patients (415 AA, 142 Caucasian, 22 others, 20 unknown). The prevalence of LVH in overall cohort was 26.7%. We noted that black had higher prevalence of LVH ( 31%) vs Whites (15.5%) while prevalence of LVH was not very different in males ( 27.9%) vs females( 25.7%) and ≥60 years of age( 27.5%) vs &lt;60 (27.3%). The analysis showed that there were statistically significant differences in the number of ACH (p-value = 0.014), HF hospitalizations (p-value = 0.019) and ER visits (p-value = 0.001) in the LVH group compared with the non-LVH group. . There were no racial, gender or age-based statistically significant differences in the impact of LVH on HF outcomes. Conclusion: Electrocardiographically determined LVH in a minority - predominant HF cohort is associated with worse outcomes. This needs to be prospectively validated in a larger cohort of HF and could serve as a prognostic marker to guide the care of HF patients.

Cardiologic Phenotypes and Natural History of FAC

Fifty years ago, the focus on the Val30Met type of the disease, in which neurologic manifestations predominate, led to the widespread notion that hereditary transthyretin-related amyloidosis (ATTR) was essentially a neurologic disease. It is now clear that ATTR is extremely heterogeneous on both genotypic and phenotypic grounds. The clinical spectrum of the disease ranges from an almost exclusive neurologic involvement to strictly cardiac manifestations. This heterogeneity is linked to several factors including specific transthyretin mutations, geographic distribution and endemic vs. non-endemic aggregation type. The existence of exclusively or predominantly cardiac phenotypes makes the recognition of the disease very challenging since it can mimic other more common causes of left ventricular “hypertrophy”. Assessment of such patients should include an active search for possible red flags that can indicate the correct final diagnosis. More in general the clinician must be aware that: • Cardiac amyloidosis (CA) should be suspected in any patient with heart failure, unexplained increased LV wall thickness and non-increased end systolic left ventricular volume • In a patient with an initial diagnosis of hypertrophic cardiomyopathy (HCM), look for the infiltrative phenotype hidden beneath the hypertrophic one! • A distinctive sign of CA is the abnormal ratio between left ventricular thickness and QRS voltages rather than low QRS voltages, alone. The absence of low QRS voltages doesn’t rule out a CA if the context is otherwise fitting and up to 20% of subjects with CA can have electrocardiographic evidence of left ventricular hypertrophy. • In an elderly man with unexplained concentric left ventricular hypertrophy, especially in the absence of hypertension, always consider the possibility of wtTTR CA! • Amyloidotic cardiomyopathy in an elderly patient with monoclonal gammopathy is not necessarily related to AL: consider the possibility of wTTR + MGUS • Longitudinal LV function can be severely depressed despite a normal LVEF and the myocardial contraction fraction is often low suggesting reduced global myocardial shortening. • Myocardial deformation is reduced in amyloidotic cardiomiopathy but the apex is generally spared • In CA, Gadolinium distribution at MRI is heterogeneous: subendocardial late gadolinium enhancement (LGE) is not the only diagnostic pattern and the absence of LGE does not exclude CA. • Bilateral carpal tunnel syndrome in a man with HCM-like phenotype on echo is highly suggestive of TTR-related CA The natural history of ATTR is only partially known, due to the rarity of the disease and its high genotypic heterogeneity. Patients with ATTR cardiomyopathy have a much more indolent course than those with AL etiology. Progression of neurological disease and heart failure are the leading causes of death. As in AL amyloidosis, in ATTR the presence of cardiac involvement is an incremental risk factor for overall and cardiovascular events. Consequently, non-Val30Met mutations, in which cardiac involvement is more frequent and severe, appear to be associated with a particularly poor prognosis, even after successful OLT . Very little is known about the underlying cause and the incidence of sudden death, which has been reported to be associated with the occurrence of advanced atrioventricular blocks, ventricular tachycardia/fibrillation, or, probably more frequently, electromechanical dissociation.

Electrocardiogram reference intervals for clinically normal wild-born chimpanzees (Pan troglodytes).

To generate reference intervals for ECG variables in clinically normal chimpanzees (Pan troglodytes). 100 clinically normal (51 young [< 10 years old] and 49 adult [≥ 10 years old]) wild-born chimpanzees. Electrocardiograms collected between 2009 and 2013 at the Tchimpounga Chimpanzee Rehabilitation Centre were assessed to determine heart rate, PR interval, QRS duration, QT interval, QRS axis, P axis, and T axis. Electrocardiographic characteristics for left ventricular hypertrophy (LVH) and morphology of the ST segment, T wave, and QRS complex were identified. Reference intervals for young and old animals were calculated as mean ± 1.96•SD for normally distributed data and as 5th to 95th percentiles for data not normally distributed. Differences between age groups were assessed by use of unpaired Student t tests. RESULTS Reference intervals were generated for young and adult wild-born chimpanzees. Most animals had sinus rhythm with small or normal P wave morphology; 24 of 51 (47%) young chimpanzees and 30 of 49 (61%) adult chimpanzees had evidence of LVH as determined on the basis of criteria for humans. Cardiac disease has been implicated as the major cause of death in captive chimpanzees. Species-specific ECG reference intervals for chimpanzees may aid in the diagnosis and treatment of animals with, or at risk of developing, heart disease. Chimpanzees with ECG characteristics outside of these intervals should be considered for follow-up assessment and regular cardiac monitoring.

Feasibility of Focused Cardiac Ultrasound in Pre-participation Screening

Objective: Current American Heart Association (AHA) guidelines for pre-participation athletic screening recommend a 12-point history and exam to minimize the risk of sudden cardiac death. We tested the hypothesis that focused cardiac ultrasound (FCU) performed and simultaneously interpreted by a cardiologist using a handheld ultrasound device would be a feasible addition. Methods: We performed pre-participation screening according to AHA recommendations on high school athletes in a multi-purpose room at their school. In addition to the standard 12-point assessment, a cardiologist simultaneously performed and interpreted a FCU on each athlete using a handheld ultrasound. Results: The mean age of the athletes was 16.6 ± 3.4 years; 68% were male. No evidence of left ventricular hypertrophy, cardiomyopathy, bicuspid aortic valve, or aortopathy was identified. Coronary ostia could not be visualized. Echocardiography added 1.35 ± 0.51 minutes to the standard exam. Conclusion: This feasibility study suggests that the addition of handheld echocardiography with real-time interpretation performed by a cardiologist to a standard AHA pre-participation screening adds less than two minutes of time to the assessment. While the study is not as comprehensive as an office based echocardiogram, it can provide valuable information which may be useful in ruling out some of the most common causes of sudden cardiac death in the young athlete or in selecting those who would benefit from further testing.

Aldosterone: Yet Another Path to Blood Pressure Variability and Target Organ Damage.

In this issue of The Journal of Clinical Hypertension, Grillo and colleagues1 demonstrated that blood pressure (BP) variability (BPV) as determined by ambulatory BP monitoring (ABPM) was greater for patients with primary aldosteronism and those with essential hypertension in comparison to patients with no hypertension. The clinical implications of their findings are significant as they demonstrate another important subgroup of patients who are at increased risk for target organ damage from BPV. In addition, these investigators provide more evidence of the clinical utility of ABPM in diagnosing BPV in at-risk patient populations. There is growing evidence from both short-term (24-hour) and long-term assessments that BPV is associated with a higher risk for stroke, myocardial infarction, and kidney disease in patients with essential hypertension.2, 3 A study of 169 hypertensive patients showed that short-term BPV was associated with increased risk for left ventricular hypertrophy, increased carotid artery intimal-media thickness, and albuminuria, and prognosis was related to the number of sites of target organ damage.4 Similarly, Tatasciore and colleagues5 demonstrated increased carotid intima-media thickness and left ventricular mass in patients with greater BPV. These findings were specific for systolic BPV while awake and were independent of mean awake BP levels.5 Long-term BPV with measurements spanning weeks, months, or years is typically assessed by patient home BP monitoring or clinic BP measurements.2 As with short-term BPV, long-term BPV has also been associated with an increased risk of target organ damage in patients with essential hypertension.2 In multiple studies, patients with greater long-term variability in their home BP measurements had a higher prevalence of cardiovascular and kidney damage2, 6 and a higher risk of cardiovascular events and mortality.2, 7-10 Significantly compounding the cardiovascular risk of BPV, hypertensive patients with primary aldosteronism appear to be even more vulnerable to target organ damage compared with patients with only essential hypertension. A study of cardiovascular outcomes compared patients with primary aldosteronism from solitary adenomas or bilateral adrenal hyperplasia with patients who had essential hypertension.11 These cardiovascular events included stroke, myocardial infarction, atrial fibrillation, and echocardiographic and electrocardiographic evidence of left ventricular hypertrophy.11 The investigators found that patients with primary aldosteronism experienced more cardiovascular events than patients with essential hypertension.11 Importantly, the excess cardiovascular event burden in the primary aldosteronism patient group was independent of BP control.11 In a subsequent study, Catena and colleagues12 showed that the prevalence of cardiovascular events was significantly greater in a group of patients with primary aldosteronism (35%) than in patients with essential hypertension (11%). This excess cardiovascular complication burden was also independent and out of proportion to the patient's BP.12 Although both of these studies did not specifically evaluate BPV, it is certainly possible that the findings of Grillo and colleagues, which implicated BPV and target organ damage, is a causative factor for the increased cardiovascular events found in patients with primary aldosteronism. Given the increased risk of target organ damage associated with BPV, it may become critical that clinicians now consider another metric to assess whether their hypertensive patients are receiving optimal antihypertensive treatment; it is now not enough to just achieve a BP below a recommended threshold. A substantial body of clinical research has demonstrated that BPV is a significant causative factor in target organ damage even when BP is adequately controlled with medical therapies. For patients with primary aldosteronism who are already more vulnerable to target organ damage than patients with essential hypertension, BPV may be an even more important factor to measure. As Grillo and colleagues demonstrated in this study, ABPM is a well-suited and useful tool to assess BPV in patients with primary aldosteronism. Currently, the use of ABPM is limited and typically confined to the diagnosis of white-coat hypertension, episodic hypertension, resistant hypertension, and hypotensive symptoms while taking antihypertensive medications and autonomic dysfunction.13-15 However, we suggest that ABPM also be considered as a tool to evaluate the extent of BPV in patients with primary aldosteronism and to determine the effectiveness of an antihypertensive regimen. Finally, the authors discuss potential mechanisms for BPV. We are left concluding that there is much more to learn, including whether the fluctuations in BP are incurring injury or simply reflecting an aspect of target organ changes. Does the fact that one finds BPV in patients with primary aldosteronism offer any clues? Certainly volume expansion is a mediator of the increase in BP in primary aldosteronism and it would seem unlikely that volume per se would vary enough to account for the BPV. A volume-expanded state, however, could sensitize BP to changes in, for example, sympathetic tone. It would be interesting to know how much BPV might decrease following removal of an adrenal tumor that produced aldosterone. An underlying role for aldosterone in the development of hypertensive states as well as hypertensive complications seem to continually widen.

Aldosterone synthase gene polymorphism in patients with hypertension combined ischemic heart disease with in various left ventricular mass

Study purpose - assessment of the relationship of levels of aldosterone and natriuretic peptide plasma aldosterone synthase gene polymorphism variants in patients with coronary heart disease (CHD) in combination with arterial hypertension (AH) at different left ventricular mass.Materials and methods. The study involved 63 male with hypertension and CHD; there were 32 men with signs of left ventricular hypertrophy (LVH) and 31 men with coronary artery disease with hypertension with a normal index of left ventricular mass. Evaluated the concentrations of aldosterone and plasma natriuretic peptide (NUP) in the relationship with characteristic of aldosterone synthase gene polymorphism.Results. It is established that the genotype CYP11В2 T/С of is associated with increased levels of aldosterone and signs of left ventricular hypertrophy. The level of LVC in the signs of LVH group was 2,1 fold higher than in patients without LVH. For patients with evidence of left ventricular hypertrophy is characterized by: the genotype of CYP11В2 T/C (62,5% of cases), the identification of the T allele (1,3 times more likely than patients without evidence of LVH) and more rarely than with normal index of left ventricular mass occurs variant CYP11В2 T/Т and more rarely prevalent allele C. Conclusion. In patients with coronary artery disease and hypertension, it is reasonable to implement in practice population genetic analysis to assess the probability the formation of left ventricular hypertrophy in the early stages of the disease.

The Effects of 17-Methoxyl-7-Hydroxy-Benzene-Furanchalcone on the Pressure Overload-Induced Progression of Cardiac Hypertrophy to Cardiac Failure

We investigated the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC), which was isolated from the roots of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z.Wei (Papilionaceae) (MKL), on the progression of cardiac hypertrophy to failure in a rat model of abdominal aortic banding (AAB)-induced pressure overloading. Endothelial dysfunction is central to pressure overload-induced cardiac hypertrophy and failure. It would be useful to clarify whether MHBFC could prevent this dysfunction. The effects of pressure overload were assessed in male Sprague–Dawley rats 6 weeks after AAB using the progression of cardiac hypertrophy to heart failure as the endpoint. The AAB-treated rats exhibited a greater progression to heart failure and had significantly elevated blood pressure, systolic and diastolic cardiac dysfunction, and evidence of left ventricular hypertrophy (LVH). LVH was characterized by increases in the ratios of heart and left ventricular weights to body weight, increased myocyte cross-sectional areas, myocardial and perivascular fibrosis, and elevated cardiac hydroxyproline. These symptoms could be prevented by treatment with MHBFC at daily oral doses of 6 and 12 mg/kg for 6 weeks. The progression to cardiac failure, which was demonstrated by increases in relative lung and right ventricular weights, cardiac function disorders and overexpression of atrial natriuretic peptide (ANP) mRNA, could also be prevented. Furthermore, MHBFC partialy rescued the downregulated nitric oxide signaling system, whereas inhibited the upregulated endothelin signaling system, normalizing the balance between these two systems. MHBFC protected the endothelium and prevented the pressure overload-induced progression of cardiac hypertrophy to cardiac failure.

Полиморфизм гена альдостеронсинтазы у больных артериальной гипертензией в сочетании с ишемической болезнью сердца при различной массе миокарда левого желудочка

Study purpose - assessment of the relationship of levels of aldosterone and natriuretic peptide plasma aldosterone synthase gene polymorphism variants in patients with coronary heart disease (CHD) in combination with arterial hypertension (AH) at different left ventricular mass.Materials and methods. The study involved 63 male with hypertension and CHD; there were 32 men with signs of left ventricular hypertrophy (LVH) and 31 men with coronary artery disease with hypertension with a normal index of left ventricular mass. Evaluated the concentrations of aldosterone and plasma natriuretic peptide (NUP) in the relationship with characteristic of aldosterone synthase gene polymorphism.Results. It is established that the genotype CYP11В2 T/С of is associated with increased levels of aldosterone and signs of left ventricular hypertrophy. The level of LVC in the signs of LVH group was 2,1 fold higher than in patients without LVH. For patients with evidence of left ventricular hypertrophy is characterized by: the genotype of CYP11В2 T/C (62,5% of cases), the identification of the T allele (1,3 times more likely than patients without evidence of LVH) and more rarely than with normal index of left ventricular mass occurs variant CYP11В2 T/Т and more rarely prevalent allele C. Conclusion. In patients with coronary artery disease and hypertension, it is reasonable to implement in practice population genetic analysis to assess the probability the formation of left ventricular hypertrophy in the early stages of the disease.

Allopurinol regresses left ventricular hypertrophy especially in those with highest left ventricular mass

Aims: Left Ventricular Hypertrophy (LVH) is common in Type 2 Diabetes (T2DM) and contributes to their high Cardiovascular (CV) event rate. LVH can be related to Oxidative Stress (OS) and allopurinol reduces OS. We therefore investigated whether allopurinol regresses LVH in patients with T2DM. Methods: We conducted a randomised, double blind, placebo controlled study in 66 T2DM patients with echocardiographic evidence of LVH. Allopurinol 600mg/day or placebo was given for nine months over the study period. The primary outcome was reduction in Left Ventricular Mass (LVM) as calculated by cardiac Magnetic Resonance Imaging (MRI) at baseline and at nine months follow-up. The secondary end-points were change in Flow Mediated Dilatation (FMD) and Augmentation Index (AIx). Results: Allopurinol significantly reduced absolute LVM (-2.65±5.91g and placebo group +1.21±5.10g (p=0.012)) and LVMI (indexed) to body surface area (-1.32±2.84g/m2 and placebo group +0.65±3.07g/m2 (p=0.017)). No significant change was seen in either FMD or AIx. Allopurinol induced LVH regression was however concentrated in those with an above median LV mass at baseline, as might be expected, as shown in Figure 1. ![Figure][1] Figure 1 Conclusion: Allopurinol regresses LVM in patients with T2DM and LVH. Importantly the effects of allopurinol on regression of LVM was more marked in the cohort with above median baseline LVM. Regressing LVH has been shown previously to improve CV mortality and morbidity. Therefore allopurinol may become a useful therapy to reduce CV events in T2DM patients with LVH and patients with more marked LVH may have more to gain [1]: pending:yes