Congestion is the main reason for hospitalization in patients with acute decompensated heart failure and is an important target for therapy. However, achieving complete decongestion can be ...challenging. Furthermore, residual congestion before discharge from hospital is associated with a high risk of early rehospitalization and death. An improved understanding of the pathophysiology of congestion is of great importance in finding better and more personalized therapies. In this Review, we describe the two different forms of congestion - intravascular congestion and tissue congestion - and hypothesize that differentiating between and specifically treating these two different forms of congestion could improve the outcomes of patients with acute decompensated heart failure. Although the majority of these patients have a combination of both intravascular and tissue congestion, one phenotype can dominate. Each of these two forms of congestion has a different pathophysiology and requires a different diagnostic approach. We provide an overview of novel and established biomarkers, imaging modalities and mechanical techniques for identifying each type of congestion. Treatment with loop diuretics, the current cornerstone of decongestive treatment, reduces circulating blood volume and thereby reduces intravascular congestion. However, the osmolality of the circulating blood decreases with the use of loop diuretics, which might result in less immediate translocation of fluid from the tissues (lungs, abdomen and periphery) to the circulation when the plasma refill rate is exceeded. By contrast, aquaretic drugs (such as vasopressin antagonists) predominantly cause water excretion, which increases the osmolality of the circulating blood, potentially improving translocation of fluid from the tissues to the circulation and thereby relieving tissue congestion.
In a trial involving 10,003 patients with suspected coronary artery disease, clinical outcomes at 2 years were not improved with an initial strategy of CT angiography, as compared with functional ...testing (exercise ECG, nuclear stress testing, or stress echocardiography).
New-onset, stable chest pain is a common clinical problem that results in approximately 4 million stress tests annually in the United States in ambulatory patients without diagnosed heart disease.
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Despite advances in cardiac testing, there is scant information on health-related outcomes and little consensus about which noninvasive test is preferable.
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As a result, current patterns of care have been questioned, including the testing of very-low-risk populations
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and the catheterization of patients who do not have obstructive coronary artery disease (CAD).
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The development of coronary computed tomographic angiography (CTA) and its application in this context has the potential to . . .
...it is said that the initial report of using M-mode ultrasound to assess left ventricular volumes was rejected by many journals as reviewers could not understand the technique 1. ...across the ...broad array of clinical syndromes in which GLS has been shown to be prognostic (the authors mention cardiomyopathies, ischemic and valvular heart diseases, heart failure and in the setting of cardiotoxic chemotherapy), and even now after many years and many papers, we do not as yet use that GLS information to drive clinical decisions. Yet, this technique, despite having achieved regulatory approval, is rarely used as no specific differential management emanates from the results no matter how high-risk they may be, and thus the imaging test result does not help clinicians move a patient's management forward.
Fluorine-18 flurpiridaz is a novel positron emission tomography (PET) myocardial perfusion imaging tracer.
This study sought to assess the diagnostic efficacy of flurpiridaz PET versus ...technetium-99m–labeled single photon emission computed tomography SPECT for the detection and evaluation of coronary artery disease (CAD), defined as ≥50% stenosis by quantitative invasive coronary angiography (ICA). Flurpiridaz safety was also evaluated.
In this phase III prospective multicenter clinical study, 795 patients with known or suspected CAD from 72 clinical sites in the United States, Canada, and Finland were enrolled. A total of 755 patients were evaluable, and the mean age was 62.3 ± 9.5 years, 31% were women, 55% had body mass index ≥30 kg/m2, and 71% had pharmacological stress. Patients underwent 1-day rest-stress (pharmacological or exercise) flurpiridaz PET and 1- or 2-day rest-stress Tc-99m–labeled SPECT and ICA. Images were read by 3 experts blinded to clinical and ICA data.
Sensitivity of flurpiridaz PET (for detection of ≥50% stenosis by ICA) was 71.9% (95% confidence interval CI: 67.0% to 76.3%), significantly (p < 0.001) higher than SPECT (53.7% 95% CI: 48.5% to 58.8%), while specificity did not meet the prespecified noninferiority criterion (76.2% 95% CI: 71.8% to 80.1% vs. 86.6% 95% CI: 83.2% to 89.8%; p = NS). Receiver-operating characteristic curve analysis demonstrated superior discrimination of CAD by flurpiridaz PET versus SPECT in the overall population, in women, obese patients, and patients undergoing pharmacological stress testing (p < 0.001 for all). Flurpiridaz PET was superior to SPECT for defect size (p < 0.001), image quality (p < 0.001), diagnostic certainty (p < 0.001), and radiation exposure (6.1 ± 0.4 mSv vs. 13.4 ± 3.2 mSv; p < 0.001). Flurpiridaz PET was safe and well tolerated.
Flurpiridaz PET myocardial perfusion imaging shows promise as a new tracer for CAD detection and assessment of women, obese patients, and patients undergoing pharmacological stress testing. A second phase III Food and Drug Administration trial is ongoing. (A Phase 3 Multi-center Study to Assess PET Imaging of Flurpiridaz F 18 Injection in Patients with CAD; NCT01347710)
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Heart failure with preserved ejection fraction (HFpEF) is a major driver of cardiac morbidity and mortality in developed countries, due to ageing populations and the increasing prevalence of ...comorbidities. While heart failure with reduced ejection fraction is dominated by left ventricular impairment, HFpEF results from a complex interplay of cardiac remodelling, peripheral circulation, and concomitant features including age, hypertension, obesity, and diabetes. In an important subset, however, HFpEF is subtended by specific diseases of the myocardium that are genetically determined, have distinct pathophysiology, and are increasingly amenable to targeted, innovative treatments. While each of these conditions is rare, they collectively represent a relevant subset within HFpEF cohorts, and their prompt recognition has major consequences for clinical practice, as access to dedicated, disease-specific treatments may radically change the quality of life and outcome. Furthermore, response to standard heart failure treatment will generally be modest for these individuals, whose inclusion in registries and trials may dilute the perceived efficacy of treatments targeting mainstream HFpEF. Finally, a better understanding of the molecular underpinnings of monogenic myocardial disease may help identify therapeutic targets and develop innovative treatments for selected HFpEF phenotypes of broader epidemiological relevance. The field of genetic cardiomyopathies is undergoing rapid transformation due to recent, groundbreaking advances in drug development, and deserves greater awareness within the heart failure community. The present review addressed existing and developing therapies for genetic causes of HFpEF, including hypertrophic cardiomyopathy, cardiac amyloidosis, and storage diseases, discussing their potential impact on management and their broader implications for our understanding of HFpEF at large.
Physiological assessment to guide the treatment of epicardial coronary stenoses has become a cornerstone of the field of interventional cardiology with an increasingly diverse range of indices ...available to the clinician. This review describes the evolution and physiologic basis of these functional indices, outlines the evidence base supporting each, and discusses their potential future role in efforts to further improve patient selection and outcomes in percutaneous coronary intervention.
Abstract Background Hypertrophic cardiomyopathy (HCM) has been prominently associated with adverse disease complications, including sudden death or heart failure death and a generally adverse ...prognosis, with annual mortality rates of up to 6%. Objectives This study determined whether recent advances in management strategy, including implantable cardioverter-defibrillators (ICDs), heart transplantation, or other therapeutic measures have significantly improved survival and the clinical course of adult HCM patients. Methods We addressed long-term outcomes in 1,000 consecutive adult HCM patients presenting at 30 to 59 years of age (mean 45 ± 8 years) over 7.2 ± 5.2 years of follow-up. Results Of 1,000 patients, 918 (92%) survived to 53 ± 9.2 years of age (range 32 to 80 years) with 91% experiencing no or only mild symptoms at last evaluation. HCM-related death occurred in 40 patients (4% 0.53%/year) at 50 ± 10 years from the following events: progressive heart failure (n = 17); arrhythmic sudden death (SD) (n = 17); and embolic stroke (n = 2). In contrast, 56 other high-risk patients (5.6%) survived life-threatening events, most commonly with ICD interventions for ventricular tachyarrhythmias (n = 33) or heart transplantation for advanced heart failure (n = 18 0.79%/year). SD occurred in patients who declined ICD recommendations, had evaluations before application of prophylactic ICDs to HCM, or were without conventional risk factors. The 5- and 10-year survival rates (confined to HCM deaths) were 98% and 94%, respectively, not different from the expected all-cause mortality in the general U.S. population (p = 0.25). Multivariate independent predictors of adverse outcome were younger age at diagnosis, female sex, and increased left atrial dimension. Conclusions In a large longitudinally assessed adult HCM cohort, we have demonstrated that contemporary management strategies and treatment interventions, including ICDs for SD prevention, have significantly altered the clinical course, now resulting in a low disease-related mortality rate of 0.5%/year and an opportunity for extended longevity.
Heart failure (HF), characterized by excessive exertional dyspnea, is a common complication within the broad clinical spectrum of hypertrophic cardiomyopathy (HCM). HF has become an increasingly ...prominent management issue with the reduction in sudden deaths due to use of implantable defibrillators in this disease. Exertional dyspnea ranges in severity from mild to severe (New York Heart Association functional classes II to IV) and not uncommonly becomes refractory to medical management, leading to progressive disability, but largely in the absence of pulmonary congestion and volume overload requiring hospitalization. HCM-related HF is most commonly due to dynamic mechanical impedance to left ventricular outflow produced by mitral valve systolic anterior motion, leading to high intracavity pressures. Surgical septal myectomy with low operative mortality (<1%) produces HF reversal and symptom relief in 90% to 95% of patients, while also conveying a survival benefit. Exercise echocardiography has assumed an important role in the evaluation of patients with HCM, i.e., by identifying candidates for septal reduction therapy with refractory HF when outflow gradients are present only with physiological exercise, distinguishing highly symptomatic nonobstructive patients as heart transplant candidates, and predicting future development of progressive HF. Notably, mortality directly attributable to HF has become exceedingly uncommon in HCM (<0.5%/year) in contrast with HF in non-HCM diseases (by 20-fold). In conclusion, HF in HCM is associated with diverse and complex pathophysiology, but a substantially more favorable prognosis than conventional non–HCM HF, and highly amenable to effective treatment options in the vast majority of patients.
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