cardiovascular-agents and Water-Electrolyte-Imbalance

With the failure of multiple trials to identify a successful therapy for heart failure with preserved ejection fraction (HFpEF), attention has shifted to defining specific phenotypes within the HFpEF spectrum in an effort to develop a targeted approach to treatment. Here we summarize the most recent studies investigating the pathophysiology and clinical features of HFpEF, and discuss recent clinical trials in the context of developing treatments that look toward the underlying cause of this disorder.. Advances in basic science and clinical research have further characterized HFpEF, identifying multiple pathophysiological mechanisms that ultimately lead to exercise intolerance and volume overload. The success of small studies focused on specific subsets of the HFpEF population has promoted the concept that there may not be one treatment strategy that can universally be applied to HFpEF.. HFpEF is associated with significant morbidity and mortality and accounts for approximately half of patients with chronic heart failure. HFpEF is a complex disease, encompassing a diverse cohort of patients and marked by the presence of multiple etiological mechanisms. The failure to develop successful therapies for the management of HFpEF may be because of inadequate standardization of the HFpEF diagnosis, overly broad inclusion criteria and inadequate differentiation of disease subtypes. Given the heterogeneity among patients with HFpEF, much of the current research is focused on understanding of pathophysiology and identifying disease phenotypes that may respond to a targeted treatment approach. Several newer approaches, including neprilysin inhibition and device therapy, offer promise for a new era of HFpEF treatment.

Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Benzazepines; Cardiovascular Agents; Heart Failure; Humans; Ivabradine; Mineralocorticoid Receptor Antagonists; Phosphodiesterase 5 Inhibitors; Renin-Angiotensin System; Spironolactone; Stroke Volume; Water-Electrolyte Imbalance

Left ventricular hypertrophy (LVH) is a cardiovascular complication highly prevalent in patients with chronic kidney disease (CKD) and end-stage renal disease. LVH in CKD patients has generally a negative prognostic value, because it represents an independent risk factor for the development of arrhythmias, sudden death, heart failure and ischemic heart disease. LVH in CKD patients is secondary to both pressure and volume overload. Pressure overload is secondary to preexisting hypertension, but also to a loss of elasticity of the vessels and to vascular calcifications, leading to augmented pulse pressure. Anemia and the retention of sodium and water secondary to decreased renal function are responsible for volume overload, determining a hyperdynamic state. In particular, the correction of anemia with erythropoietin in CKD patients is advantageous, since it determines LVH reduction. Other risk factors for LVH in CKD patients are documented: some are specific to CKD, as mineral metabolism disorders (hypocalcemia, hyperphosphatemia, low serum vitamin D levels and secondary hyperparathyroidism), others are non-traditional, such as increased asymmetric dimethylarginine, oxidative stress, hyperhomocysteinemia and endothelial dysfunction that, in turn, accelerates the process of atherogenesis, triggers the inflammation and pro-thrombotic state of the glomerular and the vascular endothelium and aggravates the process of both CKD and LVH.

Topics: Anemia; Cardiovascular Agents; Cardiovascular System; Chronic Disease; Early Diagnosis; Early Medical Intervention; Hemodynamics; Humans; Hypertension; Hypertrophy, Left Ventricular; Kidney; Kidney Diseases; Kidney Function Tests; Metabolism; Risk Factors; Severity of Illness Index; Vascular Resistance; Water-Electrolyte Imbalance

Heart failure may lead to acute kidney injury and vice versa. Chronic kidney disease may affect the clinical outcome in terms of cardiovascular morbidity and mortality while chronic heart failure may cause CKD. All these disorders contribute to the composite definition of cardio-renal syndromes. Renal impairment in HF patients has been increasingly recognized as an independent risk factor for morbidity and mortality; however, the most important clinical trials in HF tend to exclude patients with significant renal dysfunction. The mechanisms whereby renal insufficiency worsens the outcome in HF are not known, and several pathways could contribute to the "vicious heart/kidney circle." Traditionally, renal impairment has been attributed to the renal hypoperfusion due to reduced cardiac output and decreased systemic pressure. The hypovolemia leads to sympathetic activity, increased renin-angiotensin-aldosterone pathways and arginine-vasopressin release. All these mechanisms cause fluid and sodium retention, peripheral vasoconstriction and an increased congestion as well as cardiac workload. Therapy addressed to improve renal dysfunction, reduce neurohormonal activation and ameliorate renal blood flow could lead to a reduction in mortality and hospitalization in patients with cardio-renal syndrome.

Topics: Biomarkers; Cardiac Output; Cardio-Renal Syndrome; Cardiovascular Agents; Disease Progression; Diuretics; Heart; Humans; Interdisciplinary Communication; Kidney; Kidney Function Tests; Medication Therapy Management; Patient Selection; Renal Blood Flow, Effective; Renin-Angiotensin System; Risk Factors; Shock; Water-Electrolyte Imbalance

Cardiorenal syndromes (CRS) are disorders of the heart and kidneys, whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other. The management of heart failure and CRS requires an understanding not only of the pathophysiology linking these two organ systems, but also an appreciation of the pharmacological effects of agents targeting one organ and their influence on the other. For instance, treatment of cardiovascular diseases and risk factors may influence, in a beneficial or harmful way, renal function and progression of renal injury. The same is true regarding management of renal disease and associated complications, where drug therapies may influence cardiac performance or modify risk of adverse cardiovascular outcome. In this chapter, pharmacological therapies in the management of patients with acute and chronic CRS are reviewed, novel regimens for prevention and treatment of worsening renal function in acute decompensated heart failure are discussed, and the need for high-quality future studies in this field is highlighted.

Topics: Cardiovascular Agents; Heart Failure; Humans; Renal Insufficiency; Renin-Angiotensin System; Risk Factors; Water-Electrolyte Imbalance

Cardiovascular drugs can cause a variety of acid-base and electrolyte abnormalities that need to be considered when clinicians manage the large number of patients who receive these agents. Diuretic-induced metabolic alkalosis is the most common acid-base disorder observed and is associated with hypokalemia. Drug-induced hyperkalemia is the most important cause of increased potassium levels in everyday clinical practice. Multifactorial-origin diuretic-induced hyponatremia is mostly due to thiazides and should be carefully managed. This review focuses on the pathogenetic mechanisms as well as on the treatment of these metabolic derangements that are commonly encountered in patients who receive cardiovascular drugs.

Topics: Acid-Base Imbalance; Cardiovascular Agents; Electrolytes; Humans; Treatment Failure; Water-Electrolyte Imbalance

The common rhythm disturbances related to electrolyte imbalance are due predominantly to abnormalities of potassium. An understanding of the mechanism underlying these abnormalities is facilitated by a brief review of normal electrical activity during impulse propagation in cardiac tissue. Also discussed are the actions of all cardioactive and antiarrhythmic drugs on membrane permeability to ions. Lastly, the nonspecific arrhythmias associated with endocrine disturbances are outlined.

Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Cardiovascular Agents; Cimetidine; Digitalis Glycosides; Electrocardiography; Endocrine System Diseases; Humans; Hypercalcemia; Hyperkalemia; Hypocalcemia; Hypokalemia; Magnesium; Psychotropic Drugs; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Decreased pediatric survival has been reported with long-duration (>4 weeks) continuous renal replacement therapy (CRRT), though the practice has not been well-described.. Retrospective chart review in a children's hospital of all patients treated with CRRT over 2 years (2003-4), including those who underwent long (group 1) and shorter duration (group 2) therapy.. We identified 39 patients: median age was 6 years (range: 0.3-23; 7 were infants), median PRISM III score was 16 (range: 4-35), and the most frequent primary diagnosis was a stem cell transplant (in 12 out of 39). At continuous renal replacement therapy initiation, almost all patients (38 out of 39) had multiorgan dysfunction syndrome, most (35 out of 39) were being treated with at least one inotrope or vasopressor, and median fluid overload was 18% (range: 1-43%). Survival was poor (38%). Groups 1 (n = 7) and 2 (n = 32) had similar age (p = 0.44), PRISM III score (p = 0.61), and stem cell transplant diagnosis (p = 0.65). At CRRT initiation, the incidence of multiorgan dysfunction syndrome (p=0.18), inotrope or vasopressor treatment (p = 0.56), and fluid overload severity (p = 0.71) were similar. Those in group 1 had a longer mean CRRT as well as persistent cardiovascular dysfunction limiting the utility of intermittent dialysis. Survival was similar between groups (p = 1).. Critically-ill patients treated with long and shorter duration CRRT had a similar survival rate.

Topics: Adolescent; Cardiovascular Agents; Child; Child, Preschool; Critical Illness; Female; Hemofiltration; Hospital Mortality; Humans; Infant; Male; Multiple Organ Failure; New York City; Respiration, Artificial; Retrospective Studies; Stem Cell Transplantation; Survival Rate; Time Factors; Treatment Outcome; Water-Electrolyte Imbalance; Young Adult

Topics: Acute Disease; Brain Edema; Brain Ischemia; Cardiovascular Agents; Case Management; Combined Modality Therapy; Decompression, Surgical; Fever; Humans; Hyperglycemia; Hypertension; Hypoxia; Intracranial Hypertension; Pneumonia; Thrombolytic Therapy; Urinary Tract Infections; Water-Electrolyte Imbalance

We evaluated the factors related to indomethacin responsiveness of the patent ductus arteriosus (PDA) and subsequent renal and electrolyte abnormalities in a large number of low birth weight infants.. The ductus was evaluated by Doppler echocardiogram or clinical signs after the last administration of indomethacin for 2538 low birth weight infants, through the use of postmarketing surveillance data.. Multivariate logistic regression analyses demonstrated that clinical closure of PDA was significantly associated with pregnancy-induced hypertension and respiratory distress syndrome. In contrast, a 1-point increase of cardiovascular dysfunction score or a 1-day increase in postnatal age at the first indomethacin treatment decreased the responsiveness of the ductus to indomethacin. Clinical ductal reopening was significantly less likely to occur for each week of increased gestational age. Ductal reopening was more likely for each day of postnatal life at the first administration of indomethacin. Infants with preexisting renal and electrolyte abnormalities and infants whose mothers had received indomethacin tocolysis or who had chorioamnionitis were at increased risk of development of renal impairment.. Both antenatal and postnatal factors predict good or poor response to indomethacin therapy for PDA.

Topics: Cardiovascular Agents; Chorioamnionitis; Ductus Arteriosus, Patent; Echocardiography, Doppler; Female; Humans; Indomethacin; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature, Diseases; Kidney Diseases; Male; Multivariate Analysis; Pregnancy; Pregnancy Complications; Water-Electrolyte Imbalance

Topics: Acid-Base Imbalance; Cardiovascular Agents; Cardiovascular Diseases; Death, Sudden, Cardiac; Electrolytes; Humans; Survival Analysis; United States; Water-Electrolyte Imbalance