Manifestations Of Heart Failure Research Articles

Neurohumoral Pathway in Heart Failure

Heart Failure is now considered as one of the leading cause for mortality and morbidity. It is affecting several organs and cause organ damages due to the myocardial failure to pump inadequate oxygenated blood to the body including metabolites, to end organs and peripheral tissues. Heart failure results from multifactorial mechanism including neurohumoral activations including increased activity of the sympathetic nervous system, renin-angiotensin aldosteron system, vasopression and the atrial natriuretic peptide. This neurohumoral pathway has significant contribution to the development of myocardial dysfunction that lead to clinical manifestation of heart failure. Some of the markers in these pathways have now been considered as an independent predictors of prognosis in heart failure patient.

Outcomes of the minimally invasive aortic valve replacement

The OBJECTIVE was to demonstrate clinical outcomes of minimally invasive aortic valve replacement (MIAVR).MATERIAL AND METHODS. We retrospectively analyzed surgical results of treatment of patients underwent isolated AVR in our Institution between 2006 and 2018. Overall number of operations was 122; 56 of patient were operated via upper ministernotomy approach. Preoperative characteristics were similar in both groups.RESULTS. In our series MIAVR procedures had prolonged CPB and aortic cross clamping time, what significantly contributed to the increase in manifestations of heart failure in the early postoperative period, but didn’t affect the perioperative mortality and major morbidity rates. MIAVR led to reduction in postoperative blood loss and perioperative red blood cell transfusion rate. Most severe complications occurred in frail patients older than 75 years, and in those with extensive aortic annular calcification.CONCLUSION. MIAVR was the safe and reproducible surgical intervention and rarely led to significant complications in low-risk patients. Prolonged CPB time adversely affected the frequency of significant complications, especially in elderly patients. Although, selected high risk patients might benefit with MIAVR.

Ремоделирование левого желудочка у больных гипертонической болезнью

This article is devoted to the study of left ventricular remodeling processes in patients with different duration of hypertension history. The urgency of the problem lies in the fact that not only the increase in the mass of the left ventricle, but also the type of its geometric changes determines the risk of mortality of patients from cardiovascular complications. Cardiac remodeling precedes clinical manifestations of heart failure and accompanies them, as well as independently exacerbates the manifestations of diastolic and systolic ventricular dysfunction, is a serious independent prognostic risk factor for arrhythmias, coronary heart disease, strokes and sudden death. We conducted a retrospective analysis of 40 case histories of patients who were on inpatient treatment in GBUZ RM Republican hospital. Depending on the length of the disease, the subjects were divided into two groups: with the duration of the disease up to and more than 10 years. Echocardiography data were used to describe the nature of left ventricular remodeling. Our results showed that the prevalence of myocardial hypertrophy in patients with hypertension is low and is 20% in the group with anamnesis of GB<10 years and 15% — with anamnesis of GB>10 years. In the group of patients with long-term existing hypertension, more pronounced hypertrophy of the left ventricular walls is observed. In the long-term course of hypertension, the development of concentric remodeling and diastolic dysfunction of the left ventricle is an early marker of geometric restructuring of the left ventricle. Early detection of left ventricular remodeling processes is necessary for correct risk stratification and treatment tactics.

Long-Term Outcomes of Pharmacoinvasive Reperfusion Strategy Depending on the Choice of Thrombolytic Agent in ST-Segment Elevation Myocardial Infarction

There is limited information on the comparative results of using different thrombolytic drugs for pharmacoinvasive reperfusion in acute ST-segment elevation myocardial infarction (STEMI). There is special interest in comparing the efficacy of fibrin-selective and fibrin-non-selective thrombolytics. Aim. To study the prevalence of major adverse cardiovascular events and the status of patients who had STEMI and pharmacoinvasive reperfusion a year ago, depending on the choice of thrombolytic drug. Material and methods . 240 STEMI-patients undergoing pharmacoinvasive reperfusion (reference event) were divided into 4 groups depending on the choice of the thrombolytic drug (alteplase [group 1], teneteplase [group 2], fortetelizin [group 3], streptokinase [group 4]) as well as into 2 groups depending on the fibrin-specificity of thrombolytics. One year after the reference event the prevalence of major cardiovascular events (death, repeated myocardial infarction, stroke, repeated revascularization of the target vessel, and their combination) was assessed. Data of echocardiography and 24-hour ECG monitoring, indicis of rating scale of clinical state in patients with heart failure (RSCS, Mareev V.Y, 2000), results of determination of plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP) and of six-minute walk test were also analyzed. Results. One year after the reference event, patients who received fibrin-selective thrombolytics (groups 1,2, 3) compared with patients treated with fibrin-non-selective drug (group 4) had a higher left ventricular ejection fraction (49.8±7.4% vs 47,4±6.8%; p=0.048), lower index of impaired local contractility (1.19 [1.06; 1.38] vs 1.25 [1.175; 1.5], p=0.029), an end-diastolic volume (1 39.1 ±28.6 ml vs 148.7±23.9 ml; p=0.027), the size of the left atrium (39.0±4.6 mm vs 41.1 ±3.1 mm, p=0.007 ), and insignificantly lower prevalence of atrial fibrillation (1.5% vs 6.7%, p=0.068). They also showed a lower prevalence of supraventricular tachycardia (4.5% vs 13.3%, p=0.049) and ventricular extrasystoles (54.5% vs 76.7%, p=0.022) as well as the daily number of ventricular extrasystoles (4.5 [0; 32.0] vs 34, 0 [2.25; 80.25], p=0.001) with more favorable gradations and indicators of heart rate variability. Statistically significantly lower NT-proBNP level (148 [1 20; 208.5] pg/ml vs 241 [189; 287] pg/ml; p=0.000) and chronic heart failure manifestation according to RSCS (p=0.033), as well as a longer distance in the six-minute walk test (p=0.000) were found in patients treated with fibrin-selective drugs. Statistically significant differences between groups 1, 2, 3 for the study period were not found. Significant differences in the prevalence of hard clinical endpoints (death, repeated myocardial infarction, stroke, repeated revascularization of the target artery) were not found in all groups. Conclusion. More favorable clinical, laboratory and instrumental parameters were found one year after STEMI and pharmacoinvasive reperfusion with fibrin-specific thrombolytic agents as compared with fibrin-non-specific thrombolytic. All groups had no statistically significant differences in the effect on hard clinical endpoints during the entire observation period.

The role of multimodal imaging in the diagnostics of non-compaction cardiomyopathy (a clinical case)

Non-compaction cardiomyopathy is a rare heart disease of non-ischemic origin, which is characterized by increased myocardial trabecularity with deep intertrabecular recessions, which contributes to increased thrombogenicity, loss of myocardial contractility and heart failure manifestation. Despite of the increasing number of publications describing this pathology during last years, this form of cardiomyopathy remains underdiagnosed and little known for a wide range of physicians. The purpose of the study was to present the role of speckle tracking echocardiography and cardiac magnetic resonance tomography in the differential diagnosis of non-compaction cardiomyopathy. Results. It was described a clinical case of a 53-year old female with intact coronary arteries, who had been followed up for ten years with a diagnosis of dilated cardiomyopathy after the detection of a left bundle branch block. When performing standard echocardiography, a two-layer structure of the myocardium was found in the apical lateral segments of the left ventricle (LV) with the presence of hypertrabeculated internal layer and diffuse decrease in global LV contractility (three-dimensional ejection fraction 34 %). There was a decrease in LV global longitudinal strain up to 12 % measured by speckle-tracking echocardiography. Analysis of segmental myocardial deformation curves in conditions of left bundle branch block revealed the most prognostically unfavorable dyssynchrony pattern. Cardiac magnetic resonance imaging confirmed the presence of hypertrabecularity with compact to non-compact layer ratio of more than 1/2,5, which verified the diagnosis of non-compaction cardiomyopathy. Conclusions . The clinical manifestations of non-compaction cardiomyopathy are non-specific, therefore instrumental criteria play an important role in the diagnosis. Cardiac magnetic resonance imaging, three-dimensional and speckle-tracking echocardiography are reliable methods for diagnostics and prediction of this disease outcomes.

Is echocardiography mandatory for patients with chronic kidney disease?

This study aims at evaluating the prevalence of left ventricular diastolic dysfunction in a group of 319 hypertensive patients with stage 3b-4-5 chronic kidney disease (according to Kidney Disease Improving Global Outcomes classification), compared with 216 patients with essential hypertension and normal renal function. All patients underwent echocardiographic examination. Patients on stage 1-2-3a chronic kidney disease, dialysis treatment, or with previous manifestations of heart failure or other cardiovascular diseases were excluded. Patients with renal disease had significantly worse diastolic function (both considering trans-mitral flow and tissue Doppler imaging parameters). Diastolic dysfunction is found in 70.5% of the CKD group and in 41.6% of hypertensive patients (p < 0.0001). Multiple regression analysis shows an association between renal function and diastolic function (β 0.223; p < 0.0001), independent of potential confounders. Our study shows that diastolic dysfunction is highly prevalent in patients with advanced chronic kidney disease; we posit that in this population, the risk of diastolic heart failure is very high. We think that patients with a marked decrease of glomerular filtration rate (GFR) must be considered at high risk for diastolic heart failure and should have an echocardiographic examination performed, even if asymptomatic and in the absence of evident cardiovascular disease.

Soluble suppression of tumorigenisity 2 as an indicator of severity of heart failure in children with congenital acyanotic heart diseases

Objective We aimed to evaluate the role of soluble suppression of tumorigenisity 2 (sST2) as an indicator of severity of heart failure (HF) in children with congenital acyanotic heart diseases. Background HF in congenital heart diseases (CHD) is a serious problem encountered in early infancy or later. It is a significant cause of morbidity and mortality in children with CHD. SST2 is currently gaining interest as a biomarker in cardiac disease. Patients and methods A prospective comparative study was conducted on 60 children having CHD with left-to-right shunt from the Pediatric Department of Menoufia University Hospitals between August 2017 and August 2018 and were divided into two groups: group 1: 30 children with manifestation of HF. Group 2: 30 children without manifestation of HF. In addition, 25 age-matched and sex-matched healthy children were set as a control group. All children were subjected to a full clinical history and examination. Serum level of sST2 were determined. Results Level of sST2 was 82.2 ± 22.3 and 25.63 ± 19.33 ng/ml in patients with and without HF, respectively. SST2 was significantly higher in patients who developed HF than in those without HF (P Conclusion SST2 is a promising novel cardiac biomarker that could reflect the severity of HF.

Examining the impacts of 12 weeks of low to moderate-intensity aerobic exercise on depression status in patients with systolic congestive heart failure - A randomized controlled study

OBJECTIVES:Psychiatric depression disorder is common in patients with systolic congestive heart failure (HF), and both conditions share underlying pathophysiological mechanisms. The incidence rate of depression disorder has clearly increased with the increase in HF manifestations in recent decades. Depression disorder is considered an independent predisposing factor for hospitalization, disturbed functional performance, and high rates of morbidity and mortality in HF patients. This randomized controlled study was designed to examine the impacts of low- to moderate-intensity aerobic exercise training on depression status in patients with systolic congestive HF.METHODS:A total of 46 systolic congestive HF patients with depression (40-60 years of age) were randomized to receive twelve weeks of mild- to moderate-intensity aerobic exercise plus standard medical treatment (exercise group) or standard medical treatment without any exercise intervention (control group). Depression status was examined using the validated Patient Health Questionnaire-9 (PHQ9) pre- and post-intervention at the end of the study program.RESULTS:No significant differences were observed between the exercise and control groups in demographic data or clinical characteristics (p>0.05). Both study groups showed a significant reduction in depression status at the end of the 12-week intervention (p<0.05). The comparison between the mean values of the depression scores showed significant differences between the two groups after 6 and 12 weeks of the intervention, indicating a greater reduction in depression scores in the exercise group than in the control group (p<0.05).CONCLUSIONS:Twelve weeks of a low- to moderate-intensity aerobic exercise program was safe and effective for reducing depression severity in patients with systolic congestive HF. Low- to moderate-intensity aerobic training should be recommended for cardiac patients, particularly those with HF-related depression.

Implantable Cardioverter-Defibrillators are the Main Link in the Modern Concept of Sudden Cardiac Death Prevention. Problems and Prospects of the Development of the Method

The article covers the development of the problem of sudden cardiac death prevention with the implantable cardioverter-defibrillators from the moment of creation of these devices to our days. The current concept of primary prevention of sudden cardiac death, based on the severity of manifestation of heart failure and left ventricular dysfunction, is not effective enough. Its practical application is difficult because it requires mass application of implantable defibrillators, with low predictive accuracy of these criteria interms ofdevelopment of life-threatening arrhythmias. The development of methods for visualizing the myocardium, allowing to assess theseverity ofmyocardial fibrosis, as well as the possibilities of medical genetics, at the present stage, allows us to clarify indications for implantation ofcardioverter-defibrillators and thereby significantly improve the concept of preventing sudden cardiac death with these instruments.

Diagnostic capabilities of electrocardiography systolic heart failure

The contractility of the myocardium is determined by the strength and speed of contraction of the ventricles. It can be estimated from the Q-T interval of the electrocardiogram, which is an electrical systole of the ventricles. Set the change in ventricular systole by the deviation of the actual interval of Q-T from the corrected one. Elongation of ventricular systole indicates a violation of myocardial contractility, which causes the development of systolic heart failure. When comparing this indicator with the results of echocardiography, reflecting the contractility of the left ventricle, their direct dependence was established. The greater the degree of breach of myocardial contractility, the higher the percentage of the deviation of the actual Q-T interval from the corrected one. The maximum figures were recorded in patients with a global contractility disorder. This indicator can be used to detect both acute and chronic systolic insufficiency. It was established that in all patients with heart failure there was an increase in the Q-T interval. The magnitude of it depended on the degree of manifestation of heart failure. The increase in the percentage deviation of the actual value from the control occurred in patients with heart failure from I functional class to IV. Only in 1/5 of patients with heart failure of I functional class, the actual value did not differ from the control one, but under physical load, it increased significantly, which indicates the presence of latent systolic insufficiency. It is also found in patients with heart failure with a preserved ejection fraction, the development of which is associated with diastolic dysfunction. Electrocardiography can be used as a method of diagnosing systolic heart failure, which is highly informative and specific.

Treatment of horses with asthma syndrome complicated myocardiodystrophy

It has been established that in comorbid (cardiopulmonary) pathology in horses with asthma patients develop a syndrome of airway obstruction, morphofunctional changes in the erythrocyte system, impaired blood gas transmission function, increased permeability of cell membranes, which leads to complications in the form of myocardiodystrophy and cardiac failure. The use of a complex treatment regimen for horses with asthma and complicated myocardiodystrophy contributed to reducing attacks of respiratory dysfunction and symptoms of heart failure, reducing the incidence of arrhythmias and valvular regurgitation, reducing the number of neutrophils in the BAL washings, and reducing indicators characteristic of tissue hypoxia, (decrease in the number of erythrocytes, hemoglobin, hematocrit, mean corpuscular volume and mean corpuscular hemoglobin), elimination of the inflammatory process in the respiratory tract (decrease in the number of leukocytes, stab and segmented neutrophils), a decrease in the indices characterizing the integrity of the cardiomyocyte membranes (decrease in the activity of CК, CК-MB, LDH, LDH-1), restoration of diffuse capacity of the lungs (decrease in pH and increase in pO2 and pCO2 of blood). The mechanism of the positive effect of drugs that were used to treatment of horses with asthma syndrome with complicated myocardiodystrophy, which is achieved due to the cardio metabolic (cytoprotective) effect and antihypoxic ability to improve the diffusion of gases through the alveolar-capillary membrane, is established. On the one hand, it improves metabolic processes in the myocardium and, accordingly, reduces the manifestations of heart failure, and on the other hand, reduces hypoxia and respiratory failure (respiratory dysfunction), as one of the central pathogenetic mechanisms of cardiorespiratory comorbidity.

The impact of biventricular heart failure on outcomes after transcatheter aortic valve implantation.

We sought to assess the impact of different manifestations of heart failure (HF) at baseline on the short- and long-term outcomes of transcatheter aortic valve implantation (TAVI) for aortic stenosis (AS). Of 361 patients undergoing TAVI between May 2013 and April 2015, 185 (51%) showed clinical signs of HF at the time of admission. HF was diagnosed as isolated left ventricular (LV) and biventricular in 63 (34%) and 122 patients (66%), respectively. Acute device success (VARC-2) was achieved in 97% of patients without HF, in all patients with LV HF, and in 97% of patients with biventricular HF. Follow-up for a median of 427days revealed significantly poorer survival in patients with biventricular HF (1-year estimate, 72.1% [95% confidence interval, 64.0-80.2%]) than in patients with LV HF (84.5% [75.2-93.8%]; p = 0.0203) or no HF (94.3% [90.7-97.9%]; p < 0.0001). Survival in the latter two patient subgroups was statistically not different. A diagnosis of biventricular HF was associated with a hazard ratio of 2.62 (p = 0.0089) vs. no HF in the likelihood of death; NT-proBNP and the logistic EuroSCORE were not significantly associated with survival. Half of all deaths in patients with biventricular HF occurred within 42days of TAVI. Biventricular HF is a strong predictor of mortality following TAVI for severe AS. AS in patients with LV HF should be treated without delay to avoid progression to biventricular HF. Patients with AS and biventricular HF should be monitored closely after TAVI to possibly prevent early death.

Gender differences among patients with arterial hypertension and heart failure with preserved left ventricular ejection fraction

The aim – assessment of gender differences in the frequency of comorbidities, structural and functional state of the heart, arterial stiffness, pulse load and ventricular-arterial interaction in patients with hypertension and heart failure with preserved left ventricular ejection fraction.Material and methods. 115 patients were diagnosed with HFpEF II A or II B stage, II or III NYHA FC, with LV EF ≥ 50 % and signs of LV diastolic dysfunction by TTE, and were divided into 2 groups by gender (group 1 – women with AH and HFpEF, and group 2 – men with hypertension and HFpEF). The control group consisted of 58 patients matched for age, gender composition, with AH 1–2 degrees, without heart failure; they were also divided into 2 groups (groups 3 and 4, respectively). Results. The examined groups of patients did not statistically differ regarding age and, among patients with HF, men and women did not differ in frequency of II or III FC (NYHA); among men, earlier MI was noted more frequently than in women – 23 (37.1 %) vs 4 (7.5 %) (P&lt;0.001). BMI among women with or without HF was higher (30.3±5.4 vs. 29.8±4.6 and 32.0±4.5 vs. 30.0±3.2, P&lt;0.05), without differences in the frequency of obesity. In women, the average GFR was lower – 61.2±13.5 vs. 74.4±15.2 and 70.6±1.3 vs. 86.1±17.9 (by 13.3 % and 18 %, respectively, P&lt;0.001) Among patients with HFpEF, the prevalence of anemia was higher in women (16 (30.2 %) vs. 7 (11.3 %), P&lt;0.05). The distance of the 6-minute walk test was significantly less in the group of patients with HF of both genders compared with the control group (353.4±91.6 vs. 553.2±56.6 and 384.3±83.5 vs. 569.8±33.7, P&lt;0.01), with a slightly worse result among women (by 8 %, P&lt;0.01). In women with HF, compared with men, there were elevated rates of both arterial elastance Ea — 2.3±0.6 vs.1.9±0.4, P&lt;0.05 (by 17.4 %), and end-systolic stiffness Ees – 3.3±1.3 vs. 3.0±1.1, P&lt;0.05 (by 9.1 %). Despite similar values of brachial BP and central BP in women with HF, compared to men, larger PWWc-f was noted by 9.5 % (12.8±1.5 vs. 12.2±1.4, P&lt;0.05) and AIx75 by 9.2 % (37.7±12 1 vs. 34.7±8.9, P&lt;0.05).Conclusions. In the population of the examined patients with AH and HFpEF there is a tendency towards more pronounced diastolic LV dysfunction, severity of clinical manifestations of heart failure in women, in comparison with men, in the absence of gender differences. Women with HFpEF have a higher resistive and pulsative load on LV. Thus, in women with hypertension, there is an increased tendency to develop HFpEF compared to men.

7 - Glypican-1 mediates endothelial hyperpermeability in a model of acute heart failure

The lungs are active participants in heart failure (HF). Increases in LVEDP augments pulmonary capillary pressure (PCP) that causes fluid filtration resulting in dyspnea and, ultimately, frank pulmonary edema (PE). The increase in PCP does not translate to the severity of dyspnea indicating that more than Starling Forces contribute to the clinical manifestation of HF. Acute increases in PCP activate glycocalyx-dependent mechanotransduction resulting in oxidative stress, eNOS activation and endothelial hyperpermeability. Herein we investigated if glypican-1 (Gpc-1) contributes to pressure-dependent hyperpermeability and PE in a model of acute HF. The isolated perfused lung preparation was used to simulate acute HF in male CD-1 (wild type, WT) and glypican-1 knockout (Gpc-1-/-) mice. Control experiments were done setting left atria pressure (PLA) at 3cm H2O for 10min; acute HF was simulated by setting PLA at 10cm H2O for 10min. Lung edema was assessed by wet-to-dry ratio (W/D); reactive oxygen species (ROS) production and eNOS activation were assessed by lucigenin chemiluminescence, DHE fluorescence and immunoblotting, respectively. WT and Gpc-1-/- mice had similar increase in PA pressure (from 8 to 10 mmHg). Deletion of Gpc-1 protected mice from pressure-induced PE (W/D [acute HF and control]), respectively in WT: 7.3±0.3 vs 4.9±0.3 and in Gpc-1-/-: 4.8±0.3 vs 4.8±0.2), prevented pressure-dependent increase in ROS production in isolated membrane fraction and in total lung homogenates (15% and 80% increase in WT). eNOS activity was increased in WT (2-fold) and decreased in Gpc-1-/- (0.5 fold) during acute HF. L-NIO inhibited edema development in WT (W/D 6.9±0.2 and 5.1±0.1 in WT and L-NIO-perfused WT, respectively). Perfusion of Gpc-1-/- lungs with NOC9 restored the response to pressure and edema development (W/D 5.1±0.1 and 5.78±0.2 in Gpc1-/- and NOC9-perfused Gpc-1-/-, respectively). Collectively, these results suggest that Gpc-1 is required for pressure-induced endothelial hyperpermeability and PE in a model of acute HF.

Advanced Biventricular Heart Failure Leading to the Formation of a Gastric Bezoar: The Implications of Heart Failure on the Gastrointestinal Tract

While dyspnea or increasing peripheral edema come to mind when thinking of worsening heart failure (HF), seemingly unrelated symptoms such as nausea or bloating can indicate exacerbation. We highlight the significant gastrointestinal (GI) symptoms that result from HF, with emphasis on impaired gastric and intestinal motility. A 43 year-old man with cardiomyopathy (CM) presented with worsening abdominal pain, distention and nausea for 4 months. Physical exam showed jugular venous distention, peripheral edema, diminished breath sounds and a murmur. The abdomen was soft, mildly distended and tender. Labs showed B-type natriuretic peptide of 1374pg/ml. Blood gas showed a lactic acid of 3.2mmol/L. Platelet count was 66K/UL and international normalized ratio was 2.3. Total bilirubin was 4.0mg/dl with direct of 1.9mg/dl; aspartate aminotransferase of 98IU/L, alanine aminotransferase of 121IU/L and an alkaline phosphatase of 87IU/L. Computerized tomography showed wall thickening of the stomach, ascites, diffuse anasarca and thickening in the sigmoid colon. Echocardiogram showed an ejection fraction of 21-25% and global CM. Upper endoscopy revealed a gastric bezoar. The patient was given a can of Pepsi Cola and kept nil per os for repeat endoscopy, which showed resolution of the bezoar. Cardiac catheterization showed normal coronaries and reduced cardiac output (CO). Gastric emptying study confirmed gastroparesis. We look at the pathophysiology of HF and its effect on the structure and function of the GI tract. The small and large intestine display bowel wall edema with increased wall thickness leading to impaired nutrition of the enterocytes resulting in decreased absorptive function of the bowel. In the sigmoid colon, increased thickness correlates with increased concentrations of C-reactive protein and leukocytes. The intestine is one of the most perfused organs at rest, receiving 25% of the CO. At maximal exercise, gut perfusion drops to 4% of the CO. Increased sympathetic stimulation causes vessel constriction and decreased bowel perfusion. Small changes in CO lead to significant ischemia causing decreased motility and absorption and increased bowel wall permeability. Hepatic congestion from blood backup into the liver results in delayed gastric emptying, slowed gut motility, increased bowel permeability and bacterial translocation. Presented case demonstrates pathophysiology of frequently seen but often underappreciated GI manifestations of heart failure.2631_A Figure 1. CT scan of the abdomen showing wall thickening of the cardia of the stomach2631_B Figure 2. Gastric Bezoar2631_C Figure 3. Body or the stomach, on second EGD, 24 hours after can of Pepsi Cola

Resistant hypertension in elderly: a clinical manifestation of heart failure with preserved ejection fraction? retrospective single-center analysis

ABSTRACTBackground: Resistant hypertension (RHT) is defined as high blood pressure despite three antihypertensive medications one being a diuretic. RHT is a common clinical problem and as a subgroup has not been studied widely. The present study has investigated patient demographics and if the RHT might be a clinical presentation of heart failure with preserved ejection fraction (HFPEF) in elderly.Method: The outpatient data between January and June 2015 of Izmir Kemalpasa State hospital’s hypertension specialty clinic has been reviewed retrospectively. The patients with pseudo-RHT are excluded. Among 957 patients, 68 patients have been identified as true RHT with a left ventricle ejection fraction ≥50%. HFPEF is defined according to the latest guideline. Instead of a common cut-off level for NT-proBNP, age and gender-related cut-off levels have been used.Results: The mean age was 63.24 ± 12.05 years. Among 68 patients, 49 were female. While only 3 patients in younger group (8.8%) had elevated levels of NT-proBNP, 22 of older RHT patients (64.7%) had high levels. NT-proBNP levels were disproportionally high in elderly (p < 0.001) and high levels in RHT patients were related to a larger left atrial diameter (p < 0.001).Conclusion: The underlying mechanism might be different in RHT according to age. Hypervolemia might be the key factor in older RHT patients but not in younger patients. The current study suggests RHT in elderly can be a clinical presentation of HFPEF, and they should be investigated and treated accordingly. Because of single-center results and limited patients, further studies are needed.

Heart Failure in Constrictive Pericarditis Improves Rapidly with Medical Therapy in Patients with Higher Inflammatory Burden

Introduction Diastolic heart failure is the primary pathophysiologic manifestation of constrictive pericarditis. Pericardiectomy is the choice of treatment for patients who fail medical therapy. Constrictive pericarditis may be chronic or transient inflammatory or a combination of both. Medical therapy with anti-inflammatory drugs improves the pericardial inflammation in patients with increased delayed hyper-enhancement (DHE) on cardiac magnetic resonance (CMR) imaging. The evolution of constrictive physiology, heart failure manifestations and outcomes with such treatment need more study. Hypothesis We hypothesize that in inflammatory constrictive pericarditis, anti-inflammatory therapy may reduce the need for pericardiectomy by reducing inflammation and improving heart failure symptoms. We also hypothesize that patients with severe inflammation have the best response to medical therapy. Methods Consecutive patients diagnosed with constrictive pericarditis and pericardial inflammation as evidenced by their CMR and elevated inflammatory markers were included. Patients were treated as per standard of care with anti-inflammatory therapy and diuretics, and followed on an outpatient basis. CMR imaging was obtained at approximately 6 month intervals. Patients received pericardiectomy if they had persistent constrictive physiology and signs and symptoms of heart failure despite optimal therapy. Baseline characteristics, laboratory values, echocardiographic and CMR data were collected. Pericardial delayed hyper-enhancement was quantified by measuring the volume of DHE using an intensity cutoff of >6 SD above normal septal myocardium. Results A total of 44 patients with 123 CMRs were included. Pericardiectomy was performed in 19 patients. Mean age was 57.9 ± 14.5 years and 9 (28%) patients were female. Mean left ventricular ejection fraction was 59 ± 6.5 %. There were no significant baseline differences between patients who underwent pericardiectomy and those who did not. On mixed model logistic regression analysis, the odds of having constrictive physiology was reduced by 49% (95% CI: 14%–70%, P=0.011) per year of optimal medical therapy. Patients with DHE above median had a 69% lower risk of needing pericardiectomy (HR: 0.31, 95%CI: 0.10–0.95, P=0.039) (Figure. 1). Conclusions With optimal anti-inflammatory therapy, constrictive physiology resolves significantly over time. The risk of requiring pericardiectomy is lower in patients with higher pericardial delayed hyper-enhancement at baseline.

ASSESSMENT OF LEFT VENTRICULAR DYSFUNCTION IN PATIENTS WITH CORONARY HEART DISEASE DURING MINIMALLY INVASIVE SURGERY ACCORDING TO LUNG COMPUTED TOMOGRAPHY DATA

Objective: to assess whether multislice computed tomography (MSCT) of the lung can be used to diagnose the early manifestations of heart failure in patients with coronary heart disease (CHD) during minimally invasive surgical interventions.Material and methods. Lung MSCT was performed in 54 patientsaged 43 to 89 years with CHD before and after interventions. The identified group included 24 patients who had undergone coronary stenting, 26 who had cardiac pacemaker implantation, and 4 patients who had conduction pathways ablation. Left ventricular failure was assessed by hemodynamic disorders in the pulmonary circulation, by taking into account the use of known pathophysiological data. Successive lung MSCT examinations were performed before and after minimally invasive surgical interventions, by recording local densitometric changes in the lung parenchyma.Results. A procedure was proposed to objectively assess comparable ling MSCT images in the same patient in the special imaging window. The density of the lung parenchyma reduced by more than 10 Hounsfield units in 24 patients in the next periods after surgery, which was regarded as a sign of better left ventricular pumping function. Conclusion. The study showed that lung MSCT was highly sensitive in diagnosing left ventricular dysfunction in patients with CHD with improved coronary blood flow and normalized heart rate.

Temperature-sensitive sarcomeric protein post-translational modifications revealed by top-down proteomics

Despite advancements in symptom management for heart failure (HF), this devastating clinical syndrome remains the leading cause of death in the developed world. Studies using animal models have greatly advanced our understanding of the molecular mechanisms underlying HF; however, differences in cardiac physiology and the manifestation of HF between animals, particularly rodents, and humans necessitates the direct interrogation of human heart tissue samples. Nevertheless, an ever-present concern when examining human heart tissue samples is the potential for artefactual changes related to temperature changes during tissue shipment or sample processing. Herein, we examined the effects of temperature on the post-translational modifications (PTMs) of sarcomeric proteins, the proteins responsible for muscle contraction, under conditions mimicking those that might occur during tissue shipment or sample processing. Using a powerful top-down proteomics method, we found that sarcomeric protein PTMs were differentially affected by temperature. Specifically, cardiac troponin I and enigma homolog isoform 2 showed robust increases in phosphorylation when tissue was incubated at either 4 °C or 22 °C. The observed increase is likely due to increased cyclic AMP levels and activation of protein kinase A in the tissue. On the contrary, cardiac troponin T and myosin regulatory light chain phosphorylation decreased when tissue was incubated at 4 °C or 22 °C. Furthermore, significant protein degradation was also observed after incubation at 4 °C or 22 °C. Overall, these results indicate that temperature exerts various effects on sarcomeric protein PTMs and careful tissue handling is critical for studies involving human heart samples. Moreover, these findings highlight the power of top-down proteomics for examining the integrity of cardiac tissue samples.

Experience of medical treatment of neonates with Ebstein anomaly in the intensive care unit

Background: Neonates with Ebstein anomaly may remain a challenge for neonatal intensive care units due to continuously changing clinical manifestations. Maintaining an adequate cardiac output in the presence of cardiomegaly, severe cyanosis, high pulmonary vascular resistance, and rhythm disorders is a difficult task. Aim: To demonstrate the possibility of conservative management, as well as clinical and instrumental criteria of assessment of neonates with Ebstein anomaly and arterial hypoxemia and cardiomegaly. Materials and methods : Four neonates aged from 3 to 8 days of life were admitted to the neonate intensive care unit due to persistent arterial hypoxemia (SaO 2 ≤ 90%) and O2-dependence. Their cardiothoracic ratios ranged from 55 to 75% and were higher in the neonate with initial severe tricuspidal insufficiency (stage 3–4). Great Ormond Street Echocardiography (GOSE) score > 1 was found in 2 neonates with clinical manifestation of severe heart failure, arterial hypoxemia and cardiomegaly. Results : During the following 3 to 4 days, two neonates (aged 5 and 6 days) were transferred to the 2 nd stage of care due to the absence of clinical manifestations of heart failure and severe hypoxemia. In the other two cases, intensive management was necessary, with catecholamine support, oxygen therapy, infusion of prostaglandin E1, anti-arrhythmic agents, with no surgical intervention. Conclusion: The majority of symptomatic neonates with Ebstein anomaly can be stabilized in the settings of adequate conservative management. However, some of them would require transition from conservative treatment to surgical intervention. Such clinical and instrumental criteria, as SaO 2 , cardiothoracic ratio, and GOSE are the main benchmarks to choose between conservative and surgical strategy.