Diastolic Relaxation of the Heart: Basic Research and Current Applications for Clinical Cardiology

Evaluation of the Patient with Decompensated Heart Failure
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Cardiac dysfunction can be related to systolic or diastolic dysfunction, to abnormalities in cardiac rhythm, or to pre-load and after-load mismatch. Acute decompensated heart failure has also been defined by the Heart Failure Society of America as new onset of decompensated heart failure or decompensation of chronic, established heart failure with symptoms sufficient to warrant hospitalization.

Other definitions include a gradual or rapid change in signs and symptoms compatible with heart failure, resulting in a need for new and urgent intravenous therapy or urgent significant augmentation of existing therapy in patients with established or newly developed left ventricular dysfunction. Acute decompensated heart failure represents a board spectrum of clinical presentations from acute onset of pulmonary edema to a gradual worsening of symptoms in a patient with established heart failure.

The clinical classification of patients with ADHF continues to evolve and reflects ongoing changes in the understanding of the pathophysiology of this syndrome.

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The clinical syndrome of ADHF may result from disorders of the pericardium, myocardium, endocardium, or great vessels, but the majority of patients with ADHF have symptoms due to an impairment of left ventricular function. In most patients, abnormalities of systolic and diastolic dysfunction coexist. These symptoms are predominantly the result of systemic congestion due to elevated left ventricular filling pressures. Acute decompensated heart failure is known to occur in patients with preserved or reduced left ventricular ejection fraction and are a common cause of hospitalization and mortality.

Hospitalization for ADHF is independently associated with increased mortality risk.

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Patients with ADHF present frequently with other cardiovascular comorbid conditions, including coronary artery disease, hypertension, valvular heart disease, and arrhythmias, as well as noncardiovascular comorbid conditions, including renal dysfunction, pulmonary disease, and diabetes.

Several prognostic factors have been identified, including age, systolic blood pressure, serum sodium, and renal insufficiency. Timely and accurate diagnosis and assessment of ADHF is very important. Current guidelines recommend a comprehensive history and physical examination, laboratory testing, noninvasive evaluation of ventricular function, and in select patients functional and invasive testing.

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The diagnosis of ADHF is based on clinical assessment. A thorough history and physical examination, as well as initial diagnostics are essential to developing an early management strategy. Key components of the assessment include vital signs, electrolytes, renal function, and cardiac rhythm. Evaluation for precipitating factors and cardiovascular as well as noncardiovascular comorbid conditions is also important. Common symptoms include symptoms of dyspnea, orthopnea, and fatigue, as well as signs such as peripheral edema and weight gain.

The initial assessment of patients presenting with ADHF should include a thorough history and physical examination focusing on the assessment of congestion, volume status, and perfusion. In addition, common factors that precipitate ADHF, including medication and dietary noncompliance, acute coronary syndromes, uncontrolled hypertension and diabetes mellitus, atrial fibrillation and other arrhythmias, recent addition of nonsteroidal antiinflammatory drugs, pulmonary emboli, excessive alcohol or illicit drug use, thyroid dysfunction, socioeconomic considerations, and concurrent infections, must be thoroughly assessed.

The diagnosis of ADHF should be based primarily on signs and symptoms of heart failure being present. Clinicians need to determine as accurately as possible the volume status of the patient, the adequacy of circulatory support or perfusion, and the role or presence of precipitating factors and comorbid conditions. In the patient with previously established heart failure, efforts should also be directed toward understanding what has caused the apparent acute worsening of clinical symptoms. When the diagnosis of ADHF is uncertain, determination of plasma brain natriuretic peptide BNP or NT-proBNP concentration should be considered in patients being evaluated for dyspnea who have signs and symptoms compatible with heart failure.

The natriuretic peptide concentration should not be interpreted in isolation but in the context of all available clinical data bearing on the diagnosis of ADHF. However, it is important to highlight there is no single diagnostic test for ADHF because it is largely a clinical diagnosis that is based on a careful history and physical examination. The cardinal manifestations of ADHF are dyspnea, fluid retention, and fatigue. Fluid retention, commonly leads to pulmonary congestion and peripheral edema in patients with ADHF.

Patients may present with progressive weight gain, lower extremity edema, increasing dyspnea on exertion, or dyspnea at rest. Patients may note abdominal bloating or a decrease in appetite. Some patients may present with fatigue or even altered mental status. Some patients may present with sudden onset of dyspnea. Acute decompensated heart failure causes considerable morbidity and mortality, and produces a tremendous burden on health care systems worldwide.


Studies have shown that ADHF represents a period of high risk for patients, during which their likelihood of death and rehospitalization is significantly greater than for a comparable period of chronic, but stable heart failure. Prognosis is also reported to be very poor postdischarge; the mortality risk after AHDF hospitalization has been reported to be as high as Analysis of the case fatality rate for patients hospitalized with a principal diagnosis of ADHF in Scotland revealed a median survival of 1.

Studies from other countries also reveal a high mortality risk. In addition, patients also face a very high risk of rehospitalization. These statistics emphasize the need for identifying prognostic markers and clinically practical methods of risk stratification for patients hospitalized with ADHF, as well as to develop and implement more effective strategies to manage ADHF. The median age of patients was 71 to 75 years, and approximately half were women. Among hospitalized patients with ADHF, two thirds have a history of coronary artery disease and one third of these patients have a history of prior myocardial infarction.

The physical exam should focus on several key features including vital signs, the cardiopulmonary examination, neck veins, and extremities. Patients may be tachycardic and have blood pressure derangements. Hypertensive patients are more likely to have preserved systolic function, whereas hypotensive patients are more likely to be in a low-cardiac output state carrying a worse prognosis.

Pulmonary examination often reveals crackles, consistent with interstitial pulmonary edema, or wheezing.

Examination of the neck veins provides diagnostic and prognostic information. A new or changed murmur usually represents valvular abnormalities, which may reflect altered ventricular geometry.

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Abdominal examination may reveal hepatomegaly as a result of passive congestion, hepatojugular reflux or ascites. Extremity examination may reveal peripheral edema, particularly in the dependent portions of the body. Patients with acute decompensated heart failure can be classified into four groups based on the presence or absence of congestion at rest and the presence or absence of low perfusion at rest. These hemodynamic groupings can help guide therapy and are of prognostic significance.

Adapted from Stevenson LW.

1 Introduction

Dyspnea, a cardinal symptom of a failing heart, often progresses from dyspnea on exertion to orthopnea, paroxysmal nocturnal dyspnea and dyspnea on rest. Diastolic heart failure also called heart failure with preserved ejection fraction. Angiotensin-converting enzyme inhibitors ACE inhibitors open up narrowed blood vessels to improve blood flow. Redfield MM. It first shows a decrease in strain -rate and the development of PSD is observed, as well as the development of localized hypertrophy septal bulge [ 70 ].

Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart Fail. The initial evaluation of patients presenting with AHDF should include laboratory testing, including complete blood count, urinalysis, serum electrolytes including calcium and magnesium , blood urea nitrogen, serum creatinine, fasting blood glucose glycohemoglobin , lipid profile, liver function tests, and thyroid-stimulating hormone.

Cardiac troponins should be obtained to evaluate for an acute coronary syndrome. A lead electrocardiogram and chest radiograph posterior-anterior and lateral should be performed initially in all patients presenting with ADHF. Two-dimensional echocardiography with Doppler should be performed during initial evaluation of patients presenting with ADHF to assess left ventricular ejection fraction, left ventricular size, wall thickness, and valve function.

Radionuclide ventriculography can be performed to assess left ventricular ejection fraction and volumes. In select patients, coronary arteriography should be performed in patients presenting with ADHF who have angina or significant ischemia unless the patient is not eligible for revascularization of any kind.

Right heart catheterization is also indicated in select patients with ADHF. There are multiple demographic, clinical, vital sign, and laboratory parameters that have prognostic significance. A number of risk models using these variables have been derived and validated for patients presenting with ADHF Figure 2 Figure 3. Each predictive variable presented has a different point score that are then totaled and the probability of in-hospital death can be estimated. Each node is based on available data from registry patient hospitalizations for each predictive variable presented.

Percentages indicate crude mortality for each terminal node. Initial laboratory evaluation of patients presenting with AHDF should include complete blood count, urinalysis, serum electrolytes including calcium and magnesium , blood urea nitrogen, serum creatinine, fasting blood glucose glycohemoglobin , lipid profile, liver function tests, and thyroid-stimulating hormone. A normal level in an untreated patient has a high negative predictive value for ADHF, while elevated values despite optimal treatment portend a poor prognosis.

However, there is no definitive cut-off level recognized that ensures the diagnosis of ADHF. Conditions other than ADHF, which are associated with elevated BNP and NT-proBNP levels include: left ventricular hypertrophy, tachycardia, right ventricular overload, myocardial ischemia, hypoxemia, renal dysfunction, advanced age, liver cirrhosis, sepsis, and infection. Cardiac biomarkers associated with myocardial injury, such as cardiac troponin I or T, are important prognostic markers in ADHF patients and should be obtained in patients in whom acute coronary syndrome is a concern, or in whom additional risk stratification is warranted.

An increase in cardiac troponin indicates myocyte necrosis. Slight elevations in troponin have also been observed in patients with ADHF. The laboratory assessment of patients with ADHF should include a complete blood count white blood cells, hemoglobin, hematocrit, and platelets , serum electrolytes, renal indices blood urea nitrogen, creatinine, estimated glomerular filtration rate , glucose, liver function tests, and urinalysis. The presence of anemia, hyponatremia, hyperkalemia, hypokalemia, and renal dysfunction are relatively common and are important both for immediate management considerations, as well as prognosis.

Anemia is an independent predictor of in-hospital mortality in ADHF patients.

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He is additionally passionate about medical student and resident education, specifically the role of simulation, and stewarded the the PGY-1 Emergency Management curriculum in his senior year of residency. Outside of cardiology he dares to be an average climber, runner, and cyclist, and has been called both a catastrophic cook and an insufferable dinner guest by nearly all of his peers. Ethan was born in Israel and immigrated to Toronto when he was 6. He began his university studies in Astronomy and Physics but soon changed his focus to chemistry.

He completed his PhD at the University of Toronto on the Microfluidic studies of biological and chemical processes. He subsequently completed both his medical school and internal medicine training in Toronto. Throughout residency he found excitement working in the high paced environment of a coronary care unit, and has been focused on the integration of new materials into cardiovascular research.

His research interests include prevention and epidemiology with a focus on obesity related cardiovascular disease. Outside of the hospital he enjoys traveling, trying new foods, and strolling down to the harbor with his wife to get gelato. He is excited about continuing his training in Baltimore. Wendy completed both medical school and internal medicine residency at the Johns Hopkins University School of Medicine. She is currently pursuing an American Heart Association post-doctoral research fellowship studying sex differences in heart failure with preserved ejection fraction.

Her clinical and research interests are in the intersection of heart failure and preventive cardiology. After completing his internship in Kuwait, Hamied joined the Welty Lab at Harvard Medical School as a research fellow primarily focusing on cardiovascular disease prevention research. He studied the determinants of coronary atherosclerotic plaque progression measured by coronary computed tomography angiography in patients with coronary artery disease.

He then went on to complete his residency at the Beth Israel Deaconess Medical Center, where he continued to do research in cardiovascular prevention. Hamied is passionate about pursuing a career as an academic cardiologist and a physician-scientist in the field of coronary artery disease. During her undergraduate degree in Bioengineering at the University of Washington, Pranoti worked on building mobile health tools for global health settings, and on developing strategies for implanting pediatric medical devices.

Subsequently, she completed medical training at Harvard Medical School, then returned home for Internal Medicine residency at University of Washington Hospitals, and now she is looking forward to returning to the east coast for Cardiology fellowship! Ultimately, she hopes to integrate clinical experience with knowledge from research to develop tools that can positively impact the care of patients with cardiovascular disease. Pranoti enjoys dancing of all kinds, kickboxing, cooking for friends, and spending time with people she adores.