Obesity, heart failure, and pneumonia: a case report

Obesity is a widespread chronic disease of the 21 st century, characterized by excess accumulation of adipose tissue and weight gain. These patients have a significantly increased risk of cardiovascular disease and vulnerability to respiratory infections. Cardiorespiratory complications remain the leading causes of death. The combination of bilateral pneumonia (BP) and heart failure (HF), developing in the context of obesity, significantly worsens the prognosis. Brief description. This case presents describes a 60-year-old patient with obesity, bilateral pneumonia, HF, and hypertension. The main complaints were shortness of breath on exertion, cough with nummular sputum, and palpitations. The history included myocardial infarction. Body mass index was 36,8 kg/m 2 , oxygen saturation (SpO 2 ) — 86-89%. In addition, there were high respiratory rate, moderate cyanosis, reduced breath sounds, dry and wet rales. Blood pressure was 140/80 mm Hg, heart rate — 100 beats/min. Computed tomography revealed infiltrative and reticular changes in both lungs. Echocardiography revealed a decrease in the left ventricular ejection fraction to 20% and dilation. Elevated brain natriuretic peptide levels were noted. The diagnosis of bilateral pneumonia was established based on clinical and paraclinical data. Treatment was administered according to clinical guidelines. After 15 weeks, computed tomography showed following improvements: improved left ventricular (LV) contractility, decreased LV size. However, there was a decrease in glomerular filtration rate. Conclusion. This case reflects the atypical onset of bilateral pneumonia in a patient with obesity and HF: the disease manifested primarily with physical and imaging signs in the absence of laboratory markers of inflammation. This emphasizes the need for advanced diagnostics and individualized therapy, as the presence of pneumonia increases the risk of renal and cardiorespiratory complications.

Because of its wide availability, low cost, versatility, and clinical use, stress echocardiography has become increasingly recognized as a valuable tool in the assessment of patients with regurgitant valvular heart disease. Exercise testing is favored compared with pharmacological stress testing for risk stratification in asymptomatic patients and can identify what might otherwise be considered as a moderate valve disease. It has been shown to provide insights into exertional symptoms disproportionate to resting hemodynamics in these patients and to facilitate individual risk stratification. Aggravation of valvular regurgitation severity, exercise-induced pulmonary hypertension (PHT), impaired left ventricular (LV) contractile reserve, inducible ischemia, dynamic LV dyssynchrony, and altered exercise capacity, together with the development of symptoms during exercise echocardiography, provide the clinician with straightforward prognostic information, therefore enabling a more accurate definition of the optimal timing of intervention in patients with valvular regurgitation.1,2 In contrast, dobutamine stress echocardiography has little value in cases of valvular regurgitation. Dobutamine infusion is almost systematically associated with a decrease in the severity of regurgitation; however, it might be of interest in the detection of LV contractile reserve and inducible ischemia. The most common form of exercise used in conjunction with echocardiography is immediate postexercise imaging on a treadmill or upright bicycle ergometer. However, semisupine exercise testing on an appropriate tilted table allows continuous echocardiographic monitoring, which represents an advantageous tool for quantifying changes in valvular regurgitation severity, LV function, and pulmonary pressure (Table). This exercise stress echocardiography modality (ie, per-exercise echocardiography) is the most used in Europe, and we strongly suggest this approach in the setting of valvular heart disease to detect evanescent changes. A symptom-limited graded exercise test is recommended, and ≥80% of the age-predicted upper heart rate should be reached in the absence of symptoms. The test is adapted to the clinical conditions …

POSTER PRESENTATIONS

As described in Part I of this 2-part article,1 diastolic heart failure is common and causes significant alterations in prognosis. In Part II, experimental studies that have provided insight into the mechanisms that cause diastolic heart failure will be described.2–19⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓⇓ In addition, current treatment strategies and the design of future clinical trials of diastolic heart failure will be discussed. The development of truly effective therapy for diastolic heart failure depends on gaining a clear understanding of the basic mechanisms that alter diastolic function and the ability to efficiently target these mechanisms to correct these abnormalities in diastolic function. Conceptually, the mechanisms that cause abnormalities in diastolic function that lead to the development of diastolic heart failure can be divided into factors intrinsic to the myocardium itself (myocardial) and factors that are extrinsic to the myocardium (extramyocardial; Table 1). Myocardial factors can be divided into structures and processes within the cardiac muscle cell (cardiomyocyte), within the extracellular matrix (ECM) that surrounds the cardiac muscle cell, and that activate the autocrine or paracrine production of neurohormones. Each of these mechanisms are active in the major pathological processes that result in diastolic dysfunction and heart failure. Myocardial and extramyocardial mechanisms, cellular and extracellular mechanisms, and neurohumoral activation each play a role in the development of diastolic heart failure caused by ischemia, pressure-overload hypertrophy, and restrictive and hypertrophic cardiomyopathy. View this table: Table 1105290. Diastolic Heart Failure: Mechanisms ### Cardiomyocyte Diastolic dysfunction can be caused by mechanisms that are intrinsic to the cardiac muscle cells themselves. These include changes in calcium homeostasis caused by (1) abnormalities in the sarcolemmal channels responsible for short- and long-term extrusion of calcium from the cytosol, such as the sodium calcium exchanger and the calcium pump; (2) …

It has recently become firmly established that patients can experience chronic and acute heart failure with a normal ejection fraction (HFNEF).1–5 We now know this disorder is the dominant form of HF in the community, and that compared with HF with reduced ejection fraction (HFREF), it is increasing in prevalence and incidence,6 causes at least as many hospitalizations and healthcare expenditures,1,6,7 causes at least as severe chronic symptoms and reduced objectively measured exercise tolerance,4 and, once patients are hospitalized, has death rates that are similarly grim.1,6 Until recently, however, we have invested nearly all our resources into understanding the pathophysiology and treatment of HFREF. As a result, a physician managing a patient with HFREF can rely on practice guidelines that are solidly supported by dozens of large trials demonstrating substantial improvements in each of the meaningful HF outcomes: mortality, hospitalizations, exercise intolerance, and reduced quality of life. When the patient instead has HFNEF, there is relatively little information about pathophysiology or treatment to guide the physician. This fact is reflected in outcomes, which a recent study indicates are improving in patients with HFREF but worsening in those with HFNEF.6 This disconcerting imbalance is magnified by sex and age, as the large burden of HFNEF falls primarily on older women.1,2,6 Article p 2051 In the present issue of Circulation , Westermann and colleagues8 report a welcomed and important study aimed at addressing the dearth of information about the pathophysiology of HFNEF. They studied 70 very well-characterized patients with documented symptoms of HF, normal left ventricular (LV) EF, and no other detectable cause for their symptoms, including pulmonary and ischemic heart disease. The investigators used a conductance catheter to measure pressure–volume loops during supine rest, handgrip exercise, and atrial pacing to 120 bpm. They …

The preceding article in this series1 reviewed evidence as to why age-associated changes in the central arterial system are risky with respect to vascular disease. In a similar vane, the focus of this article is on the potential link between age-associated changes in the heart and clinical cardiac disease outcomes. Left ventricular hypertrophy, heart failure, and atrial fibrillation increase dramatically with age (Figure 1). The prevalence of left ventricular hypertrophy (LVH) also increases with rising blood pressure and body mass index, a measure of obesity.2–4 Whether identified by electrocardiography or echocardiography, left ventricular hypertrophy has been shown to be associated with increased risk for coronary heart disease, sudden death, stroke, and overall cardiovascular disease.4,5 Figure 1. A, Prevalence of echocardiographic left ventricular hypertrophy (LVH) in women according to baseline age and systolic blood pressure. B, Prevalence of echocardiographic LVH in men according to baseline age and systolic blood pressure. Both A and B are reprinted from Levy D, Anderson KM, Savage DD, et al. Echocardiographically detected left ventricular hypertrophy: prevalence and risk factors: the Framingham Heart Study. Ann Intern Med . 1988;108:7–13. C, Prevalence of heart failure by age in Framingham Heart Study men (light bars) and women (dark bars). Reprinted from Ho KK, Pinsky JL, Kannel WB, et al. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol 1993;22:6A–13A. D, Prevalence of AF by age in subjects from the Framingham Heart Study. Reprinted from Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke . 1991;22:983–988. It has been increasingly appreciated that the development of heart failure with apparently preserved systolic function, as evidenced by a “normal” ejection fraction, occurs in about one-third to one-half of older patients with heart failure.6–9 In a …

Commentary: Renal Effects of Cyclooxygenase-2-Selective Inhibitors

To evaluate the impact of a decrease in glomerular filtration rate (GFR) on the prognosis of patients with chronic heart failure (CHF), to analyze real clinical practice regarding the frequency of prescribing pathogenetic therapy for CHF, achieving target dosages depending on the gradation of GFR in patients included in the CHF Register of the Tyumen region. The analysis included medical data of 4077 patients (1662 men and 2415 women) with NYHA class I-IV CHF who underwent examination and treatment in medical organizations of the Tyumen region for the period from January 2020 to May 2023. Criteria for inclusion in the register: proven heart failure. Chronic kidney disease (CKD) was assessed by GFR calculated using the CKD-EPI formula (ml/min/1.73 m2). The primary end point was defined as death from all causes. GFR<60 ml/min/1.73 m2 was recorded in 34.6% of patients, more common in women (40.2 and 26.6%, respectively; p<0.001). When dividing patients into phenotypes according to LVEF, no statistically significant differences were found in the distribution of patients according to GFR. In patients with HFrEF and HFpEF GFR<45 ml/min/1.73 m2 was associated with an increased risk of meeting the endpoint. Analysis of prescribed pathogenetic therapy showed that in patients with HFrEF, the frequency of prescription of ACE inhibitors, â-blockers and MRA decreased (p=0.023, 006 and 0.01, respectively), and ARNI, on the contrary, increased with a decrease in GFR (p=0.026). In patients with HFpEF, a similar trend towards a decrease in the frequency of prescription of ACEIs and MCBs with a decrease in GFR (p<0.001) remained, but it was compensated by an inversely proportional increase in the frequency of prescription of ARBs (p<0.001). 100% of the target dosage is achieved in more than 90% of patients taking MRA across the entire LVEF range. While for â-blockers and ARNI/ACE/ARB the percentage of patients receiving the full therapeutic dosage of drugs is significantly lower. When analyzing target dosages of pathogenetic drugs, gradations of achieved doses were distributed evenly throughout the entire range of GFR. GFR<60 ml/min/1.73 m2 occurs in every 3 patients with CHF across the entire range of LVEF. A decrease in GFR worsens the prognosis of patients with both HFrEF and HFpEF, increasing in direct proportion with the severity of the stage of CKD. Inclusion of patients in the monitoring program within the framework of the CHF service allows the treatment to be significantly brought closer to optimal drug therapy, at the same time, certain efforts are required to overcome difficulties with titration to target dosages.

The global epidemic of type 2 diabetes mellitus (T2DM) has substantial implications for cardiovascular disease–related morbidity and mortality.1 The prevalence of T2DM in patients with heart failure (HF) is high, with strong and independent association between T2DM and incident HF observed in multiple prospective studies and in randomized-controlled clinical trials. In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), which enrolled subject’s ≥55 years of age with hypertension and ≥1 risk factor, patients with T2DM had a 2-fold risk for HF hospitalization or death after adjustment for other risk factors (RR, 1.95). The association with T2DM was independent of coronary artery disease and at least equivalent in magnitude and greater than that for electrocardiographic left ventricular (LV) hypertrophy.2 All measures of glycemia including fasting, postprandial, measures of insulin resistance, and hemoglobin A1c (HbA1c) have been associated with risk of developing HF, with the association extending to both HF with preserved ejection fraction and to HF with reduced ejection fraction.3,4 A substantial body of evidence from preclinical studies, endomyocardial biopsies in humans and more recently with cardiac MRI, support increased myocardial stiffness in T2DM related to alteration in extracellular matrix. There are multiple proximate mediators that have been hypothesized to play a role including advanced glycation end product deposition and reactive oxygen species that may increase myocardial stiffness during diastole, by cross-linking collagen or by enhancing collagen formation.5,6 Another pernicious proximal mediator is the elevation in postprandial lipids, such as remnant lipoproteins, characteristic of atherogenic dyslipidemia, a highly prevalent abnormality in T2DM, that may result in direct myocellular deposition of lipid, leading to microcirculatory dysfunction, alteration in substrate use and mitochondrial dysfunction.7,8 Indeed, positron emission tomography studies show reduced myocardial glucose uptake in favor of fatty acid …

Treatment of Diabetes in People with Heart Failure

Kidneys are one of the most crucial organs in heart failure, which provides a basis for understanding the nature of the disease and helps to implement appropriate treatment. A reduction in glomerular filtration rate (GFR) allows for early diagnosis of subclinical renal disease. Data from the Heart Failure Pilot Registry, conducted in 29 cardiology centres in Poland in the years 2010-2011, allow to identify this population. Purpose: The aim of the study is to analyze a series of clinical data of patients with heart failure and GFR below 60 ml/min/1,73m2. Material: Data of 780 patients included in the Heart Failure Pilot Registry in which GFR could be calculated from the MDRD formula. Value of serum creatinine necessary for calculation of GFR came from a stable period of the disease. Results: GFR in the study population ranged from 10 to 384 ml/min/1,73m2. Median GFR was 74 ml/min/1,73m2. In 253 people (23% of population) GFR values didn't exceed 60 ml/min/1,73m2. The largest group of patients with GFR below 60 ml/min/1,73m2 were elderly (76±8 years vs. 62±12 years, p<0.001) women (41% vs. 29%, p<0,005), with ischemic etiology of heart failure (64% vs. 53%, p=0,001), higher NYHA class (3.0±0.7 vs. 2.7±0.8, p<0.001), with more frequent incidence of hypertension (74% vs. 59%, p<0.001) and chronic obstructive pulmonary disease (15% vs. 10%, p<0.05). In laboratory studies, beyond the elevated levels of creatinine (median – 1,4mg/dl) and urea, emphasized lower hemoglobin in blood serum (12.8±2.1 g/dl vs. 13.6±2.3 g/dl, p=0.03), frequent proteinuria (27% vs. 14%, p<0.01) and slightly higher serum potassium (4.5±0.7 mmol/l vs. 4.4±0.5 mmol/l, p=0.001). Smaller dimension of the left ventricle in diastole (56±11 mm vs. 59±10 mm, p=0.04) was accompanied by a similar left ventricular ejection fraction (42±14% vs. 41±14%, p=0.34) on echocardiography. The clinical picture often showed symptoms of pulmonary congestion at the time of hospital admission (64% vs. 50%, p<0.001), and during outpatient treatment (38% vs. 21% (p<0.01) at almost the same heart rate and blood pressure values. Jugular vein congestion was also observed more frequently (16% vs. 10%, p<0.05). In the 12-month follow-up death occurred in 44 patients (17%) with GFR not exceeding 60 ml/min/1,73m2 and 37 patients (7%) with a higher GFR (p<0,001). Conclusions: A significant decrease in GFR accompanied by heart failure in every third patient and is observed even in the stable phase of the disease. Identification of these patients is essential to optimize treatment given the significantly higher 12-months mortality.

Cardiac Autonomic Nerve Stimulation in the Treatment of Heart Failure

Aim. To identify cardiorenal relationships and related characteristics in individuals with various cardiomyopathies.Material and methods. An analysis of 267 patients with cardiomyopathy (CMP) was conducted, of which 204 (76,4%) were men. There were dilated CMP (DCM), hypertrophic CMP (HCM), alcoholic (ACM), ischemic CMP (ICM) and inflammatory CMP (InCM). We assessed the relationships between glomerular filtration rate (GFR) and CMP forms and following echocardiography parameters: ejection fraction (EF), left ventricular (LV) end-systolic (ESD) and end-diastolic dimensions (EDD), left ventricular wall thickness (LVWT), right ventricle (RV), left and right atria.Results. Among individuals with CMP, a significant decrease in GFR was found in DCM, ICM, and HCM. In men, there was a positive relationship between GFR and EF and a negative relationship between GFR and ESD in DCM (r=0,317, p=0,012 and r=-0,269, p=0,036) and ICM (r=0,359, p=0,017 and r=-0,660, p=0,007). In women, no relationships between GFR and EF were found. In women with DCM, a strong positive relationship between GFR and LVWT (r=0,894, p=0,041) was found. In women with ICM, a negative relationship between GFR and RV (r=-0,650, p=0,003) and ESD (r=-0,829, p=0,042) was found. In women with DCM and ICM, only the RV parameter was included in the regression equations with the dependent variable GFR, while in men, all echocardiography parameters were included. In the general HCM group, there was a negative correlation between GFR and LVWT (r=-0,571, p=0,021). In the HCM group, a negative relationship between GFR and EDD was recorded in young men (r=-0,520, p=0,027) and in young women (r=-0,750, p=0,05).Conclusion. In individuals with DCM, ICM, and HCM, a decrease in GFR is observed compared to ACM and InCM at the corresponding age. In men with DCM and ICM, a positive correlation of GFR with EF is recorded, and in women with ICM, a negative relationship of GFR with RV. Therefore, sex-specific relationships between GFR and echocardiography parameters in men and women reflect one or another adaptive model of cardiovascular remodeling in CMP. Left ventricular remodeling in CMP with thickening or thinning is associated with a decrease in GFR in both men and women.

NONSTEROIDAL antiinflammatory drugs (NSAIDs) inhibit prostaglandin synthesis. Because renal blood flow depends on prostaglandin, particularly when circulating blood volume is decreased, a recommendation has been made that NSAIDs be withheld before surgery because of the risk of renal dysfunction. 1 However, there has been no report of perioperative renal dysfunction attributable to preoperative administration of NSAIDs, and a recent review has endorsed preoperative administration of NSAIDs for minor outpatient procedures and a combined multimodality drug therapy including NSAIDs after surgery. 2 The authors report a case of perioperative acute renal failure after lumbar discectomy in a young patient who was taking ibuprofen preoperatively.

Does cardiac resynchronization therapy benefit patients with right bundle branch block: cardiac resynchronization therapy has a role in patients with right bundle branch block.