Reversal Of Left Ventricular Hypertrophy Research Articles

COMPARISON OF CARDIAC STRUCTURAL AND FUNCTIONAL CHANGES BETWEEN SURGERY AND MEDICATION TREATMENT IN PATIENTS WITH PRIMARY ALDOSTERONISM BASED ON ECHOCARDIOGRAPHY

Objective: Conducted a systematic meta-analysis on the changes in follow-up parameters of echocardiography in patients with primary aldosteronism after surgery and drug treatment, in order to explore their differences. Design and method: We conducted the PubMed, Embase, and Cochrane library databases for English full-text articles on the follow-up study of echocardiography parameters in PA patients before and after surgery and drug treatment published from its establishment until June 1, 2023,Perform meta-analysis on the included studies using RevMan software. Results: A total of 515 PA patients (>18 years old) were included in 4 studies, including the surgical group (n=303) and the medication group (n=212), 2 short-term follow-up studies (average follow-up time of 1 year), and 2 long-term follow-up studies (average follow-up time of 3.7 years). Surgery treatment had better performance in improving cardiac contractile function, The main manifestation is the reversal of left ventricular hypertrophy (LVMI: M=-2.6, p=0.047), while there is no significant improvement in cardiac diastolic function (E/A: M=+0.06, p=0.51); In long-term follow-up studies, surgery and medical treatment still showed significant benefits in reducing blood pressure (surgical group: -14 ± 6 mm Hg/-9 ± 10 mm Hg, p<0.001; drug group: -10 ± 12mmHg/-11 ± 9mmHg, p<0.001). Interestingly, the surgical group and drug group did not show better blood pressure control effects than short-term follow-up (p=0.56), Surgery (LVMI: M=-12.6, p=0.01)and medication (LVMI: M=-11.9, p=0.01])can significantly improve left ventricular hypertrophy in patients, with no significant difference (P=0.143). Although surgery (E/A: M=+0.14, p=0.125) and medication (E/A: M=+0.09, p=0.2) can numerically improve diastolic function, there is no statistically significant difference. Conclusions: Both medication and surgical treatment can reverse the damage to the heart structure and function in PA patients. In the short term, surgical treatment has a more significant reversal of cardiac function, especially in left ventricular hypertrophy, but in the long term, there is no significant difference between medication and surgical treatment.

Thyroid gland and heart: a cardiologist’s view on an endocrinological pathology. Review

The review of the literature considered the mechanism of action and the role of thyroid hormones (TH) on cardiovascular hemodynamics and, subsequently, on changes in the myocardial structure. A brief description of the genomic and non‑genomic mechanisms of thyroid hormones is provided. The mechanisms of thyroid hormones’ effects on the development of arterial and pulmonary hypertension, atrial fibrillation are highlighted. Attention is focused on the fact that congestive heart failure of the dilatation type develops against the background of hyperthyroidism. A possible connection between thyroid hyperfunction and Takotsubo stress‑induced cardiomyopathy was investigated. The impact of subclinical hyperthyroidism on the development and progression of cardiac pathology is illustrated. The mechanism of influence of hypothyroidism on the parameters of the lipid spectrum, acute phase proteins, insulin sensitivity, but not only the contractile function of the myocardium was considered. Changes in the electrical activity of the heart and its structural and functional changes were determined. Attention is focused on the importance of achieving euthyroidism in both hyperthyroidism and hypothyroidism. Stress‑induced Takotsubo cardiomyopathy is closely related to the hyperthyroid state and is often accompanied by the development of cardiogenic shock. Hyperthyroidism is associated with an increased risk of permanent atrial fibrillation and hypercoagulability. The achievement of euthyroid state can result in the reversal of left ventricular hypertrophy and decrease in the heart chamber dilatation. Even subclinical hyperthyroidism increases the risks of overall mortality and cardiovascular events, especially in the elderly persons. Patients with hypothyroidism are characterized by the development of anemia, dyslipidemia, decreased sensitivity to insulin, which is associated with endothelial dysfunction. In hypothyroidism, in contrast to hyperthyroidism, the risk of atrial fibrillation development is lower due to an increase in the arrhythmogenic threshold, but more typical disorders include sinus bradycardia, atrioventricular blocks of various degrees and prolongation of the QT interval, which are associated with the early development of impaired myocardial relaxation. For patients with thyroid pathology, the achievement of euthyroidism is mandatory to ensure cardio‑ and vasoprotection.

Reversible cardiac function and left ventricular hypertrophy in a Chinese man with mitochondrial myopathy: a case report

BackgroundMitochondrial myopathies (MMs) are a group of multi-system diseases caused by abnormalities in mitochondrial DNA (mtDNA) or mutations of nuclear DNA (nDNA). The diagnosis of mitochondrial myopathy (MM) is reliant on the combination of history and physical examination, muscle biopsy, histochemical studies, and next-generation sequencing. Patients with MMs have diverse clinical manifestations. In the contemporary literature, there is a paucity of reports on cardiac structure and function in this rare disease. We report a Chinese man with MM accompanied with both acute right heart failure and left ventricular hypertrophy.Case presentationA 49-year-old man presented with clinical features suggestive of MM, i.e., ophthalmoparesis, weakness of the pharyngeal and extremity muscles, and respiratory muscles which gradually progressed to respiratory insufficiency. He had a family history of mitochondrial myopathy. He had increased levels of serum creatine kinase and lactate. Muscle biopsy of left lateral thigh revealed 8% ragged red fibers (RRF) and 42% COX-negative fibers. Gene sequencing revealed a novel heterozygote TK2 variant (NM_001172644: c.584T>C, p.Leu195Pro) and another heterozygous variant (NM_004614.4:c.156+958G>A; rs1965661603) in the intron of TK2 gene. Based on these findings, we diagnosed the patient as a case of MM. Echocardiography revealed right heart enlargement, pulmonary hypertension, left ventricular hypertrophy, and thickening of the main pulmonary artery and its branches. The patient received non-invasive ventilation and coenzyme Q10 (CoQ10). The cardiac structure and function were restored at 1-month follow-up.ConclusionsThis is the first report of reversible cardiac function impairment and left ventricular hypertrophy in a case of adult-onset MM, nocturnal hypoxia is a potential mechanism for left ventricular hypertrophy in patients with MM.

Exploring the Interactive Role of Parathyroid Hormone and Sodium Intake in Inducing Cardiac Hypertrophy in Rats: A Novel Study.

Background and objectives Previous research has suggested that hyperparathyroidism and excessive salt intake may contribute to the development of cardiac hypertrophy. This study aimed to investigate the relationship and underlying mechanisms between parathyroid hormone (PTH) and salt intake in the development of left ventricular hypertrophy (LVH). Additionally, the study sought to determine whether captopril intervention could reduce the impact of sustained PTH stimulation and excessive salt intake on LVH. Methodology We employed 40 eight-week-old male Sprague-Dawley rats, which were randomly assigned to eight groups: a sham group, a PTH group, a low-salt group (0.6% NaCl), a high-salt group (8% NaCl), a PTH + low-salt group, a PTH + high-salt group, a PTH + low salt + captopril group, and a PTH + high salt + captopril group. The rats were continuously infused with recombinant PTH (1-34) (2 pmol/kg per hour) via an osmotic pump for two weeks and were administered varying concentrations of saline for gavage over two weeks, according to their group. We monitored changes in blood pressure, measured heart weight, left ventricular wall thickness, and myocardial histological morphology, and assessed the relative expression of type III collagen. Results The PTH + high-salt group displayed a significant increase in blood pressure, heart weight, and left ventricular posterior wall thickness (P＜0.05), in addition to myocardial cell hypertrophy and increased Col III expression (P＜0.05), compared to other groups. Captopril intervention significantly reduced blood pressure (P＜0.05), ameliorated myocardial tissue morphology changes, and significantly decreased Col III expression (P＜0.05) but did not entirely reverse the increase in heart weight and left ventricular posterior wall thickness (P＞0.05). Conclusions Our findings suggest that the co-intervention of PTH and high salt can lead to an increase in blood pressure, heart weight, myocardial cell hypertrophy, LVH, and myocardial fibrosis levels in Sprague-Dawley rats. Captopril intervention can lower blood pressure and alleviate pathological myocardial tissue changes and myocardial fibrosis but cannot completely reverse LVH.

Experimental renal transplantation in rats improves cardiac dysfunction caused by chronic kidney disease while LVH persists.

Chronic kidney disease (CKD) causes congestive heart failure (CHF) with systolic dysfunction and left ventricular hypertrophy (LVH), which is a major contributor to increased mortality in CKD patients. It remains unclear whether cardiovascular changes that occur during the course of CKD can be reversed when renal function is restored by transplantation. To investigate this, chronic kidney disease was established in F344 rats by subtotal nephrectomy (SNx) for 8 weeks, followed by transplantation of a functional kidney from an isogenic F344 donor. SNx rats without transplantation and sham-operated animals served as controls. Renal function was assessed before and throughout the experiment. In addition, cardiac ultrasound was performed at weeks 0, 8, 12 and 16. At the end of the experiment, intra-arterial blood pressure was measured and kidneys and hearts were histologically and molecularly examined. Eight weeks after SNx, rats developed marked renal dysfunction associated with significant glomerulosclerosis and tubulointerstitial fibrosis, but also an increase in left ventricular mass. After transplantation, renal function normalized but relative heart weight and ventricular mass as assessed by ultrasound scans showed no reduction compared with SNx controls. However, left ventricular wall thickness, fractional shortening and ejection fraction was normalized by renal transplantation. At 8 weeks after kidney transplantation, cardiac expression of BNP and FGF23 was also at levels comparable to healthy controls, whereas these factors were significantly increased in SNx rats. Cardiac fibrosis, as measured by fibronectin mRNA expression, was completely normalized, whereas cardiac fibronectin protein was still slightly but not significantly increased in transplanted animals compared to controls. In addition, the myofibroblast marker collagen 1, as assessed by immunohistochemistry, was significantly increased in SNx rats and also normalized by renal transplantation. Interestingly, CD68+ macrophages were significantly reduced in the hearts of SNx rats and in transplanted animals at slightly higher levels compared to controls. Restoration of renal function by kidney transplantation normalized early cardiac changes at most functional and molecular levels, but did not completely reverse LVH. However, further studies are needed to determine whether restoration of renal function can also reverse LVH at a later time point.

Research Progress on the Efficacy and Safety of Spironolactone in Reversing Left Ventricular Hypertrophy in Hemodialysis Patients.

The mineralocorticoid receptor antagonist spironolactone has been shown to improve cardiac function and reverse left ventricular hypertrophy in heart failure patients, but there are no consistent findings on the efficacy and safety in hemodialysis patients. Abnormal aldosterone secretion plays a critical role in the formation of left ventricular hypertrophy. Because of the existence of "aldosterone escape", the routine use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers does not completely inhibit aldosterone secretion. Low-dose spironolactone (25 mg/d) has been found in small-sample clinical studies to have a significant positive impact with respect to decreasing left ventricular mass index, increasing left ventricular ejection fraction, reversing left ventricular hypertrophy, and improving cardiovascular function while still being safe. More prospective multicenter clinical trials with large sample sizes are needed, however, to provide convincing evidence.

The impact of mTOR inhibitors in the regression of left ventricular hypertrophy in elderly kidney transplant recipients.

End-stage kidney disease is frequently associated with left ventricular hypertrophy (LVH), a condition more prevalent in the elderly, that may increase mortality after renal transplantation (RTx). Previous studies suggested that mTOR inhibitors (mTORi) can improve LVH, but this has never been tested in elderly kidney transplant recipients. In this prospective randomized clinical trial, we analyzed the impact of Everolimus (EVL) on the reversal of LVH after RTx in elderly recipients (≥60 years) submitted to different immunosuppressive regimens: EVL/lowTacrolimus (EVL group, n=53) or mycophenolate sodium/regularTacrolimus (MPS group, n=47). Patients performed echocardiograms (Echo) up to 3 months after RTx and then annually. At baseline, mean age was 65±3 years in both groups and LVH was observed in 63.6% of patients in EVL group and in 61.8% of MPS group. Last Echo was performed at mean time of 47 and 49 months after RTx in EVL and MPS groups, respectively (P=.34). LVH regression was observed in 23.8% (EVL group) and 19% (MPS group) of patients (P=1.00). Mean eGFR, blood pressure, and use of RAS blockers were similar between groups throughout follow-up. EVL did not improve LVH in this cohort, and this lack of benefit may be attributed to concomitant use of TAC, senescence, or both.

Echocardiographic predictors of left ventricular reverse remodeling after aortic valve replacement in patients with paradoxical aortic stenosis

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Paradoxical aortic stenosis (AS) is low-flow (SVi ≤ 35ml/m2) , low- gradient (Mean PG ≤ 40mmHg) severe aortic stenosis (AVA < 1cm2) in patients with preserved ejection fraction (EF ≥ 50%) usually associated with female gender, advanced age, small body size and history of hypertension. Left ventricular (LV) reverse remodeling presents with LV hypertrophy reversal following aortic valve replacement (AVR) and is associated with better long term prognosis. Purpose The purpose of our study was to asses echocardiographic predictors of better outcome in patients with paradoxical severe AS following AVR. Methods Detailed transthoracic echocardiographic (TTE) evaluation with left ventricular strain analysis was performed using 2D Philips Epique 7 in patients with severe aortic stenosis with AVR indication before and 4 months after the intervention. Results Among 75 patients with severe AS and indication for AVR, 20 (31, 7%) were paradoxical AS with low- flow, low –gradient and preserved ejection fraction. Sixty percent were female and eighty percent had hypertension where all echocardiographic parameters improved following AVR including improvement of LV global longitudinal strain (LS) as well as reduction of left ventricular mass indicating left ventricular reverse remodeling (Figure 1). The patients with paradoxical AS compared to the other forms of severe AS had the lowest values for MAPSE and s’TDI before and after AVR. Independent predictors of LV reverse remodeling before AVR were end systolic LV volume (ESV) , AVA/BSA and the number of segments with LS < 13%. Conclusion Paradoxical severe AS is associated with worse post AVR prognosis compared to the high gradient severe AS. Echocardiographic predictors of LV reverse remodeling in patients with paradoxical severe AS following AVR are LV ESV, AVA/BSA and number of segments with LS < 13%. Timely diagnosis and AVR referral of patients with paradoxical severe AS is of major importance in the management of aortic valvular disease. Abstract Figure. Descriptive of 20pts with paradoxical AS Abstract Figure. Predictors of LV reverse remodeling

Reversal of hypertensive heart disease: a multiple linear regression model.

Background: The development of left ventricular hypertrophy in primary hypertension increases cardiovascular mortality and morbidity. Reversal of left ventricular hypertrophy through therapeutic control of blood pressure reduces the risk of adverse cardiovascular incidents. Objective: In our study, we explored for the determinants of left ventricular hypertrophy regression. Methods: A cohort (n=217) of patients with hypertensive left ventricular hypertrophy was identified by screening consecutive patients in medical outpatient unit. The primary inclusion criteria were (i) Blood pressure more than140/90 mm of Hg (ii) Left Ventricular Mass Index more than 115 and 95 gm/m2 for males and females respectively. Left Ventricular Mass Index was determined by echocardiography at the time of recruitment and after 24 weeks of standard pharmacotherapy. The change in Left Ventricular Mass Index was modelled using multiple linear regression with both categorical and continuous explanatory variables. The effect of drug therapy on change in Left Ventricular Mass Index was tested in the model with dummy coded variables for the treatment categories. Results: In simple linear regression, the variables significantly correlating with change in Left Ventricular Mass Index were baseline Left Ventricular Mass Index (r=0.62, p<0.001), change in systolic blood pressure (r=0.22, p=0.001), change in mean blood pressure (r=0.16, p=0.02), baseline systolic blood pressure (r=0.15, p=0.02), age (r=0.12, p=0.09) and diabetes (r=0.12, p=0.09). The best fit model (r2=0.408) retained baseline Left Ventricular Mass Index (β=0.59, p<0.001), change in systolic blood pressure (β=0.14, p=0.01) and diabetes (β=-0.104, p=0.05) as the significant predictors. Introduction of treatment effect into the model non-significantly increased the fit of the model (r2=0.414, p=0.27-0.98). Conclusions: Pre-treatment Left Ventricular Mass Index and reduction in systolic blood pressure were the major determinants of left ventricular hypertrophy regression. We also observed that there is lesser left ventricular hypertrophy regression in diabetic patients, warranting future research to explore glycaemic control as a modifiable factor in left ventricular hypertrophy reversal.

Anabolic Androgenic Steroids Induce Reversible Left Ventricular Hypertrophy and Cardiac Dysfunction. Echocardiography Results of the HAARLEM Study.

Background: The use of anabolic androgenic steroids (AAS) is not uncommon among strength athletes. Several cross-sectional studies have linked AAS use to heart disease, but a causal role for AAS is not certain and it is unknown whether cardiac changes are reversible.Methods: Men of at least 18 years old intending to start an AAS cycle on short notice were included for comprehensive 3D echocardiographic examination before (T0), at the end of the cycle (T1), and 1 year after inclusion (T2) after a recovery period. Details of the AAS cycle performed and the use of other performance and image-enhancing drugs (PIEDs) as well as illicit drug use were recorded. Trend analysis and multivariable regression analysis were performed with mixed effects linear models.Results: Thirty-one subjects were included. Between start (T0) and end of the cycle (T1), after a median AAS cycle duration of 16 weeks, 3D left ventricular ejection fraction declined with 4.9% (CI −7.2 to −2.5, P < 0.001), E/A-ratio declined with−0.45 (CI −0.69 to −0.21, P < 0.001), and 3D left atrial volume increased with 9.2 ml (CI 2.9–15.4, P = 0.004). Left ventricular mass increased with 28.3 g (CI 14.2–42.4, P < 0.001) and was positively correlated with AAS average weekly dose. After a median recovery time of 8 months (T2), all parameters returned to baseline.Conclusion: AAS induce left ventricular hypertrophy and impaired systolic and diastolic function in amateur strength athletes. The structural cardiac changes are positively associated with AAS dose and complete recovery occurred after AAS were discontinued.

Potential of valsartan+sacubitril therapy in hypertensive heart disease

The course of hypertension is often complicated by left ventricular hypertrophy (or hypertensive heart disease, HHD). The main “corridor” of natural HHD is development of heart failure with preserved ejection fraction (HFpEF). With HFpEF, the bioavailability of natriuretic peptides (NP) is significantly reduced, as a result of which the activity of cGMP-PKG signaling pathway, which plays a key role in maintaining normal diastolic function, weakens. It is possible to increase the activity of this pathway using the neprilysin inhibitor sacubitril. In case of HFpEF, the greatest efficacy from valsartan+sacubitril therapy should be expected in patients with severe concentric LVH, who have the most pronounced natriuretic peptide deficiency. Valsartan+sacubitril therapy has a clear hypotensive effect, causes a reversal of left ventricular hypertrophy and fibrosis. Since no effective treatment has yet been found for HFpEF, the main way for HHD treatment should be to prevent the diastolic dysfunction progression, which justifies valsartan+sacubitril therapy starting from the early/ asymptomatic stages.

Reversible left ventricular hypertrophy and congestive heart failure due to suspected myocarditis in a cat in the course of FLUTD

A 2.5-year-old castrated male domestic shorthair cat with a past pertinent history of FLUTD treatment 8 days earlier was presented during the night due to apathy and anorexia. Radiographs, ECG, blood pressure measurement and echocardiography revealed left-sided congestive heart failure, left ventricular concentric hypertrophy, left atrial dilation, severe diastolic dysfunction, hypotension, and vagotonus-associated sinus bradycardia with a first degree AV-block as well as a right bundle brunch block. NT-ProBNP and troponin I concentrations were elevated (NT-ProBNP > 1500 pmol/l, Troponin I 32.87 ng/ml). Presumptive diagnosis was acute myocarditis. Bartonella henselae PCR and Toxoplasma gondii IgM titer were negative. Initial IgG titer amounted to 1:32 (reference range: < 1:32) and on later testing this was negative. FeLV and FIV tests exhibited negative results. Coronavirus testing was not performed because the cat was vaccinated accordingly. A metastatic infection with Proteus mirabilis, which had been isolated from the urine, appeared possible. Alternatively, a hypersensivity reaction to drugs or a stress-induced myocarditis was taken into consideration. The hospitalized cat was treated with furosemide (initialy and in the course of further treatment), theophyllin (initially), continuous infusion with lactated Ringer's solution, pimobendan, and the addition of enrofloxacin to the ongoing amoxicillin/clavulanic acid administration. After 4 days, the cat's general condition improved satisfactorily and blood pressure returned to normal range. Left ventricular hypertrophy resolved, however, diastolic dysfunction as well as left atrial dilation persisted. Within the next 8 weeks, echocardiographic findings and cardiac biomarkers returned to near normal values. All medication was tapered and finally discontinued. During the last recheck examination 7 months following initial presentation, no cardiac changes were apparent.

Clinical efficacy of L-arginin aspartate in complex treatment of patients with essential arterial hypertension with concomitant type 2 diabetes mellitus

Objective. Investigate directly the clinical efficacy of L-arginine aspartate in the treatment of patients with essential arterial hypertension (EAG) and type 2 diabetes mellitus (DM).&#x0D; Materials and methods. The study included 43 patients with EAG II in combination with type 2 DM. The mean age of patients was 55,7±0,6 years, of which 20 (46,5 %) were men and 23 (53,5 %) were women. The duration of the disease on the EAG averaged 8,4±0,4 years, on type 2 DM – 6,5±0,5 years. A comprehensive clinical, laboratory and instrumental examination was carried out. All patients were divided into two groups. Patients in both groups received ramipril 5-10 mg a day in combination with amlodipine 5-10 mg a day and antidiabetic drugs (metformin, gliclazide or a combination thereof) as basic therapy. Patients in group 2 (n=22) were additionally prescribed the drug L-arginine aspartate orally 3 g 3 times a day for 4 weeks. The course of treatment was repeated after 2 months.&#x0D; Results and discussion. In group 2 there was a more pronounced tendency to decrease the average daily and night blood pressure levels, in particular diastolic (3,2 and 2,9 mm Hg; p&gt;0,05) and heart rate (by 17,3 %; p&lt;0,05). The use of L-arginine aspartate significantly improved systolic (ejection fraction increased by 7,1 % vs 4,4 % in group 1; p&lt;0,05) and left ventricular (LV) diastolic function (Em/Am increased by 48,8 % vs 34,7 % in group 1; p&lt;0,05), a decrease in the size of the left atrium (10,2 % vs 8,3 % in group 1; p&lt;0,05) and the reversal of LV hypertrophy (index LV myocardial mass decreased by 20,1 % against 15,9 % in group 1; p&lt;0,05). Additional administration of L-arginine aspartate also led to a decrease in fasting and postprandial plasma glucose (4,9 % and 7,0 %; p&lt;0,05, respectively) than the use of basic therapy alone. At the same time in group 2 there was a decrease in microalbuminuria by 27,6 % (p&lt;0,05) and an increase in glomerular filtration rate by 11,4 % (p&gt;0,05).&#x0D; Conclusions. L-arginine aspartate should be used in patients with EAG in combination with type 2 DM and microalbuminuria to increase the cardio- and nephroprotective efficacy of basic therapy.

Zi Shen Huo Luo Formula Enhances the Therapeutic Effects of Angiotensin-Converting Enzyme Inhibitors on Hypertensive Left Ventricular Hypertrophy by Interfering With Aldosterone Breakthrough and Affecting Caveolin-1/Mineralocorticoid Receptor Colocalization and Downstream Extracellular Signal-Regulated Kinase Signaling.

Left ventricular hypertrophy (LVH) is an important characteristic of hypertensive heart disease. Renin-angiotensin system (RAS) blockers have been shown to be effective drugs for the reversal of LVH. Clinical and experimental studies have shown that Zi Shen Huo Luo Formula (ZSHLF) can improve the efficacy of perindopril in the treatment of hypertensive LVH, but its mechanism is unclear. This study aimed to investigate the possible mechanism to improve the efficacy of perindopril. First, we identified 23 compounds in ZSHLF by ultra performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) analysis, among which ferulic acid, caffeic acid, vanillic acid, berberine, rutin, quercetin, kaempferol, stachydrine, and tiliroside have been reported to reduce blood pressure and exhibit cardioprotective effects. Second, we treated spontaneously hypertensive rats (SHRs) with perindopril and ZSHLF for 12 continuous weeks and found that chronic use of perindopril could increase the aldosterone (ALD) levels and cause aldosterone breakthrough (ABT). ZSHLF combined with perindopril reduced the ALD levels, interfered with ABT, decreased blood pressure, improved left ventricular diastolic dysfunction, and decreased the collagen volume fraction; these effects were superior to those of perindopril alone. In vitro experiments, ALD-induced cardiomyocytes (H9c2 cells) and cardiac fibroblasts were treated with ZSHLF-containing serum, which suppressed ALD-induced cardiomyocyte hypertrophy and cardiac fibroblast proliferation, increased mineralocorticoid receptor (MR) and Cav-1 colocalization and decreased phosphorylated epidermal growth factor receptor (pEGFR) and phosphorylated extracellular signal-regulated kinase (pERK) protein expression the cells. In conclusion, ZSHLF can interfere with ABT and affect the pathological role of ALD by affecting MR and Cav-1 interactions and EGFR/ERK signaling pathway. These effects represent a possible mechanism by which ZSHLF improves the efficacy of angiotensin-converting enzyme inhibitors (ACEIs) in hypertensive LVH treatment. However, the major bioactive components or metabolites responsible for the effects and the implications of these findings in patients need further verification.

Early reversal cardiac with esmolol in hypertensive rats: The role of subcellular organelle phenotype.

Our group has previously shown that short-term treatment (48 h) with esmolol reduces left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs). However, we do not know the mechanism that explain this effect. The aim of this study was to assess the role that the subcellular organelle phenotype plays in early cardiac reverse after short-term treatment with esmolol. 14-Month-old male SHRs were randomly assigned to receive esmolol (300 μg/kg/min) (SHR-E) or vehicle (SHR). Age-matched male Wistar-Kyoto rats (WKY) served as controls. After 48 h of treatment, an ultrastructural analysis of heart tissue (left ventricle) was performed. We studied cardiomyocyte ultrastructural remodeling of subcellular organelles by electronic microcopy in all groups. SHR group showed significant morphometric and stereological changes in mitochondria and subcellular organelles (cytoplasm and nucleus, myofibril structure, mitochondria structure, Z-Disk, intercalated disk, T-system and cystern), and also changes in the extracellular matrix (collagen) with respect to WKY group. Esmolol significantly improved the morphology and stereology mitochondrial, reduced the organelle phenotype abnormalities but no produced changes in the extracellular matrix with respect to SHR group. Interesantly, parameters of mitochondria (regularity factor, ellipsoidal form factor and density of volume), and all parameters of subcellular organelles returned to the normality in SHR-E. Our results show that left ventricular hypertrophy reversal after short-term treatment with esmolol is associated with reversal of subcellular organelle phenotype.

Mineralocorticoid Receptor Antagonists in Primary Aldosteronism.

Primary aldosteronism is the most common causes of secondary hypertension. Patients suffering from this clinical syndrome have an increased cardiovascular risk and target organ damage. Mineralocorticoid receptor antagonists are the optimal pharmaceutical option for the management of such patients. The study aimed to assess the effects of mineralocorticoid receptor antagonist in the treatment of patients with primary aldosteronism. We conducted an in-depth review of the literature and comprehensive identification of the clinical studies investigating the efficacy of mineralocorticoid receptor antagonists in individuals with primary aldosteronism. Mineralocorticoid receptor antagonists result in significant improvement in blood pressure and serum potassium level among patients with primary aldosteronism. Moreover, mineralocorticoid receptor antagonists reverse left ventricular hypertrophy, albuminuria, and carotid intima-media thickness. However, a high risk for atrial fibrillation remains among subject with primary aldosteronism in such agents. Mineralocorticoid receptor antagonists are recommended as the first-line treatment in patients with bilateral primary aldosteronism. In patients with unilateral aldosterone-producing adenoma, adrenalectomy should be preferred. However, existing data presents significant limitations and is rather inconclusive. Future randomized control trials are required in order to illustrate the field.

Effect of individualized antihypertensive therapy on the blood pressure and left ventricular hypertrophy of hypertensive patients with coronary heart disease

Objective: To investigate the effect of individualized antihypertensive therapy on the blood pressure and left ventricular hypertrophy (LVH) of hypertensive patients with coronary heart disease (CHD). Methods: We conducted a prospective study from Sep. 2014 to Dec. 2015 in Chinese PLA General Hospital. A total of 650 patients complicated with non-dipper or reverse-dipper hypertension and CHD were enrolled. All the participants were divided into non-dipper (n=259) and reverse-dipper (n=391) group according to their 24h ambulatory blood pressure monitoring (ABPM) reports. Patients who took short-acting antihypertensives changed their medicine to long-acting ones. Patients who had already taken long-acting antihypertensives switched to nighttime or added antihypertensives at night. Self-measured home blood pressure was recorded before going to bed and in the morning. All patients were regularly followed up by face-to-face surveys and clinic BP was recorded every 3 months. After 1 year's follow-up, the effect of individualized antihypertensive treatment on circadian rhythm of blood pressure was evaluated by 24h ABPM. The effect of individualized antihypertensive treatment on LVH was evaluated by echocardiography. Results: After 1 year's individualized antihypertensive therapy, the clinic BP and 24h ABPM of the patients were decreased. BP rhythm in 44% of the non-dipper and 57% of the reverse-dipper patients restored to normal. LVH were returned to normal in 44% of the non-dipper patients and and 48% of the reverse dipper patients, respectively. Left ventricular mass index (LVMI) were (59±12) kg/m(2.7) vs (48±10) kg/m(2.7) (P<0.01), and (63±13) kg/m(2.7) vs (48±11) kg/m(2.7) (P<0.01) respectively in non-dipper and reverse-dipper group before and after individualized antihypertensive treatment. Conclusion: Individualized antihypertensive intervention of abnormal blood pressure circadian rhythm can effectively restore the circadian rhythm of blood pressure and reverse LVH in hypertensive patients with CHD.

Impact of left ventricular hypertrophy on long-term clinical outcomes in hypertensive patients who underwent successful percutaneous coronary intervention with drug-eluting stents.

Left ventricular hypertrophy (LVH) is associated with increased risk for vascular events and mortality. This study investigated 8-year clinical outcomes of hypertensive patients with LVH who underwent percutaneous coronary intervention (PCI) with drug-eluting stents (DES) compared with hypertensive patients without LVH.A total of 1704 consecutive hypertensive patients who underwent PCI from 2004 to 2014 were enrolled. We classified them into either the LVH group (n = 406) or the control group (without LVH, n = 1298). LVH was defined by LV mass index > 115 g/m2 in men and > 95 g/m2 in women. After propensity score matched (PSM) analysis, 2 PSM groups (366 pairs, n = 732, c-statistic = 0.629) were generated.For up to 8 years, the LVH group showed a higher incidence of cardiac death (4.4% vs 1.2%, log-rank P = .023, hazard ratio: 3.371, 95% confidence interval: 1.109–10.25; P = .032) compared with the control group. However, there were no significant differences between the 2 groups in the incidence of total death, myocardial infarction, revascularization, and major adverse cardiac events up to 8 years.LVH in hypertensive patients who underwent successful PCI with DES was associated with higher incidence of cardiac death up to 8 years of follow-up. More careful managements and clinical follow-up are needed and treatment strategies should specifically focus to target prevention and reversal of LVH in hypertensive patients.

A prospective study of various anti hypertensive drugs on reversal of left ventricular hypertrophy in hypertensive Bangladeshi population

Regression of ventricular hypertrophy is the restoration of normal ventricular structure and physiology after the hypertrophy has developed. It has been clearly demonstrated that once left ventricular hypertrophy (LVH) is diagnosed, it represents a strong blood pressure independent risk factor for cardiovascular morbidity and mortality.This prospective observational study was carried out in Department of Cardiology, BSMMU, Dhaka to compare the effectiveness of different anti-hypertensive agents in reducing left ventricular hypertrophy (LVH) in hypertensive Bangladeshi population involving 95 patients with clinically diagnosed hypertension. The duration of study was from July 2005 to Tune 2008. Out of these 95 patients, 20 were included in beta-blocker(BB) group, 14 in angiotensin converting enzyme inhibitor(ACEi) group, 20 in beta-blocker(BB) + diuretic(DD) group, 14 in angiotensin converting enzyme inhibitor(ACEi) + diuretics(DD) group, 13 in beta-blocker(BB) and angiotensin enzyme inhibitor(ACEi) group and 14 in beta-blocker(BB) + angiotensin converting enzyme inhibitor(ACEi) + diuretic(DD) group. patients were followed-up at 8 weeks, 6 months, 1 year and at 2 years. A baseline M-mode echocardiography was done to document LVH. Among three groups of anti-hypertensive drugs, angiotensin converting enzyme inhibitor alone has been found to be most effective as compared to beta blockers when used alone than in combination groups (Beta blocker plus ACEi plus Diuretics or Beta blocker plus ACEi). Although, statistically not significant, a clear benefit has been shown in all groups in terms of LVH regression.Bangladesh Med J. 2016 Sep; 45 (3): 156-159

Screening and Treatment for Subclinical Hypertensive Heart Disease in Emergency Department Patients With Uncontrolled Blood Pressure: A Cost-effectiveness Analysis.

Poorly controlled hypertension (HTN) is extremely prevalent and, if left unchecked, subclinical hypertensive heart disease (SHHD) may ensue leading to conditions such as heart failure. To address this, we designed a multidisciplinary program to detect and treat SHHD in a high-risk, predominantly African American community. The primary objective of this study was to determine the cost-effectiveness of our program. Study costs associated with identifying and treating patients with SHHD were calculated and a sensitivity analysis was performed comparing the effect of four parameters on cost estimates. These included prevalence of disease, effectiveness of treatment (regression of SHHD, reversal of left ventricular hypertrophy [LVH], or blood pressure [BP] control as separate measures), echocardiogram costs, and participant time/travel costs. The parent study for this analysis was a single-center, randomized controlled trial comparing cardiac effects of standard and intense (<120/80 mm Hg) BP goals at 1 year in patients with uncontrolled HTN and SHHD. A total of 149 patients (94% African American) were enrolled, 133 (89%) had SHHD, 123 (93%) of whom were randomized, with 88 (72%) completing the study. Patients were clinically evaluated and medically managed over the course of 1 year with repeated echocardiograms. Costs of these interventions were analyzed and, following standard practices, a cost per quality-adjusted life-year (QALY) less than $50,000 was defined as cost-effective. Total costs estimates for the program ranged from $117,044 to $119,319. Cost per QALY was dependent on SHHD prevalence and the measure of effectiveness but not input costs. Cost-effectiveness (cost per QALY less than $50,000) was achieved when SHHD prevalence exceeded 11.1% for regression of SHHD, 4.7% for reversal of LVH, and 2.9% for achievement of BP control. In this cohort of predominantly African American patients with uncontrolled HTN, SHHD prevalence was high and screening with treatment was cost-effective across a range of assumptions. These data suggest that multidisciplinary programs such as this can be a cost-effective mechanism to mitigate the cardiovascular consequences of HTN in emergency department patients with uncontrolled BP.