Congestive heart failure historical perspective

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ACC/AHA Guideline Recommendations Initial and Serial Evaluation of the HF Patient Hospitalized Patient Patients With a Prior MI Sudden Cardiac Death Prevention Surgical/Percutaneous/Transcather Interventional Treatments of HF Patients at high risk for developing heart failure (Stage A) Patients with cardiac structural abnormalities or remodeling who have not developed heart failure symptoms (Stage B) Patients with current or prior symptoms of heart failure (Stage C) Patients with refractory end-stage heart failure (Stage D) Coordinating Care for Patients With Chronic HF Quality Metrics/Performance Measures
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Specific Groups: Special Populations Patients who have concomitant disorders Obstructive Sleep Apnea in the Patient with CHF NSTEMI with Heart Failure and Cardiogenic Shock
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Overview

Heart failure (HF) is known to be recognized as a disease since ancient times. Italian Egyptologist Ernesto Schiaparelli reported the first case of decompensated heart failure (HF) in the remains of a tomb in the Valley of the Queens over 3500 years ago the remains are now housed in the Egyptian museum in Turin, Italy. They belonged to an Egyptian dignitary named Nebiri who lived under the reign of the 18th dynasty Pharaoh Thutmose III (1479–24 BC). Various other features of HF such as cardiac hypertrophy and coronary atherosclerosis were also known to Egyptians. In China, ‘the Yellow Emperor’s Classic of Internal Medicine’ described edema as early as 2600 B.C. The medieval Arab scholar Ibn Sina, known to the West as Avicenna (980–1037), had a reputation as an authority on heart disease. His treatise entitled ‘Kitab al-Adviyt-al-Qalbiye’ or ‘The book on drugs for cardiac diseases’ discusses therapies for difficulty in breathing, palpitation, and syncope. Widely used in the West in a Latin translation in the 14th century, the treatise remains in the Galenic tradition of humours. In 1628 when William Harvey clearly described circulation and elucidated hemodynamic abnormalities occurring in HF. Röntgen discovered x-rays in 1895 and allowed a more thorough understanding of maladaptive changes occurring in HF patients.In the 1940s and 1960s the advent of cardiac catheterization and cardiac surgery furthered our understanding of HF. The 1960s was also the decade that saw the emergence of LV assist devices (LVADs), beginning in 1961 when Dennis and co-workers uses a roller pump to assist the left ventricle. From the mid-1970s, the availability of vasodilators provided a means to reduce afterload in order to increase cardiac efficiency and cardiac output in HF

Historical Perspective

Ancient Times

• Italian Egyptologist Ernesto Schiaparelli reported the first case of decompensated heart failure (HF) in the remains of a tomb in the Valley of the Queens over 3500 years ago the remains are now housed in the Egyptian museum in Turin, Italy. They belonged to an Egyptian dignitary named Nebiri who lived under the reign of the 18th dynasty Pharaoh Thutmose III (1479–24 BC).
• Andreas Nerlich, a pathologist from Munich, Germany, demonstrated the presence of pulmonary edema by examining histopathological findings in the lungs.
• Various other features of HF such as cardiac hypertrophy and coronary atherosclerosis were also known to Egyptians.
• In China, ‘the Yellow Emperor’s Classic of Internal Medicine’ described edema as early as 2600 B.C.
• Greek and Roman texts also contain descriptions of HF, although edema, dyspnea and anasarca, the most common manifestations described in these texts, could be attributed to other causes than HF.
• Hippocratic corpus while describing rales, a common finding in HF patients as: ‘When the ear is held to the chest, and one listens for some time, it may be heard to see the inside like the boiling of vinegar’ (translation by A. Katz). He also demonstrated a method to drain this fluid through a hole drilled in the ribcage. However, at that time, there seem to have been no understanding about why the fluid had accumulated.
• Erophilus and Erasistratus performed human dissections and experiments and commented that the heart contracts but believed that the arteries contained air and that blood was confined to the veins.
• Even Galen, a Greek physician during the second century was of the view that the heart was just a source of heat failing to understand its role as a pump. He almost certainly described atrial fibrillation (AF) and indeed palpated the arterial pulse, a technique that had been used for prognosis millennia earlier by the Egyptians.However, Galen believed that the pulse was transmitted by the arterial walls rather than by blood flowing through the lumen.
• The medieval Arab scholar Ibn Sina, known to the West as Avicenna (980–1037), had a reputation as an authority on heart disease. His treatise entitled ‘Kitab al-Adviyt-al-Qalbiye’ or ‘The book on drugs for cardiac diseases’ discusses therapies for difficulty in breathing, palpitation, and syncope. Widely used in the West in a Latin translation in the 14th century, the treatise remains in the Galenic tradition of humours.

Recognition of the Heart's Pump Function (17th to 20th Century)

• In 1628 when William Harvey clearly described circulation and elucidated hemodynamic abnormalities occurring in HF.
• A few years later, a description of HF due to tamponade and to mitral stenosis was published.
• In the mid-18th century, Lancisi noted that valvular regurgitation leads to ventricular dilatation, which weakens the heart but he appreciated that the ventricle cavity does not enlarge in aortic stenosis.
• Subsequently, the occurrence of cardiac hypertrophy, both eccentric and concentric, and the existence of acute and chronic HF as well as the role of adaptive and maladaptive changes in the failing heart were described. Bedside examination techniques such as palpation, percussion, and auscultation were used to confirm these findings.
• Röntgen discovered x-rays in 1895 and allowed a more thorough understanding of maladaptive changes occurring in HF patients.
• Distinction between the various forms of cardiac enlargement continued into the 20th century.
• In 1918 E.H. Starling described his ‘Law of the Heart’ which forms the basis of modern Frank-Starling curves.

The Advent of Cardiac Catheterization and Cardiac Surgery (1940's-1960's)

• In the 1940s and 1960s the advent of cardiac catheterization and cardiac surgery furthered our understanding of HF.
• In the decades before the 1980s, the only attempt to explain the changes occurring in HF was related to the back/forward theories and treatment was based on bed rest, inactivity and fluid restriction.
• On the pharmacological side, only digitalis and diuretics were prescribed, and HF research often concentrated more on the kidney than on the heart. With the publcation of of ‘Families of Starling Curves’ by S.J. Sarnoff the concept of contractility originated, based on the possibility of shifting from one curve to another, and the ‘contractile’ state of the heart became a major regulator of cardiac performance.
• Research was concentrated on understanding the cause of low contractility in HF. Thus, the role of energy starvation and abnormal calcium movement gained rapid popularity and stimulated efforts to develop inotropic drugs that were more powerful than digitalis. However, all clinical trials of inotropic drugs were stopped prematurely because the agents did more harm than good and none had a positive effect on survival.
• A few years later, cardiac glycosides were also found not to improve survival in patients with HF in sinus rhythm.
• The 1960s was also the decade that saw the emergence of LV assist devices (LVADs), beginning in 1961 when Dennis and co-workers uses a roller pump to assist the left ventricle.

Recognition of Role of Renin-Angiotensin Aldosterone System (1970's-1980's)

• From the mid-1970s, the availability of vasodilators provided a means to reduce afterload in order to increase cardiac efficiency and cardiac output in HF
• In 1986, The Vasodilator-Heart Failure Trial (V-HeFT I), was conducted by J. Cohn and colleagues and demonstrated that, despite short-term hemodynamic improvement, afterload reduction alone may benefit patients in the form of improved survival.
• In 1980's HF became recognized as a neuroendocrine disease. The chronic activation of renin-angiotensin-aldosterone system and increase in catecholamines in untreated HF patients became known to scientists.
• As a result, angiotensin converting enzyme inhibitors (ACEIs) and beta-blockers were successfully introduced as a treatment for HF.
• Later, pharmacological therapies which counter the unchecked RAAS activation such as spironolactone were also introduced as add-on therapies to ACEI and beta-blockers.

Heart Failure as a Syndrome and Introduction of implantable cardioverter—defibrillators (1990's-2000's)

• With the introduction of ACEI, beta blockers and mineralocorticoid antagonists for the management of HF, it became apparent that HF may begin with the affecting the heart but the consequences tend to involve other organ systems such as the lungs, peripheries, kidneys and even the liver.
• Since arrhythmias were recognized as bein fatal in HF patients, ICDs were introduced during the early 21st century for management of HF.
• Later, this was reinforced by introduction of implant-based multi parameter telemonitoring, chronic vagal stimulation and wireless implanted devices for better outcomes.
• In the late 1990's researchers began to understand the molecular basis of HF due to major advancements in the field of epigenetics and understanding of role of micro RNAs. Micro RNAs have been implicated in regulation of gene transcription and protein formation by silencing the messenger RNA, and are deeply involved in HF. In addition, miRNAs could be useful biomarkers for severity of HF and need of transplantation.
• Recently, researchers have attempted to explore the possibility of stem cell transplantation for improvement of outcomes in HF patients.

Modern Era and Landmark Events in the Treatment of HF

• The latest breakthroughs surrounding HF have been in the form of new pharmacological treatments. The PARADIGM -HF study, in which a dual angiotensin receptor and neprilysin inhibition (ARNi) with sacubitril/valsartan (LCZ696) significantly improved prognosis compared with treatment with the enalapril in HFrEF, suggest that neuroendocrine modulation deserves more attention in management.
• The options available for treatment of HFpEF lag behind the advances made in treating HFrEF patients. Sacubitril/valsartan is currently being investigated in HFpEF. Phase II trial data with sacubitril/valsartan indicate that the ARNi reduces nt-proBNP and left-atrial size in patients with HFpEF.
• The PARAGON-HF trial will study the efficacy and safety of ARNi compared with valsartan.
• The RELAX-AHF trial using serelaxin, a recombinant peptide of the human relaxin-2 hormone, showed promising results in 2013. In this phase II/III trial, continuous infusion of serelaxin for 48 hrs within 16 hrs of presenting to the hospital lead to an improvement in dyspnea, congestive symptoms, and initial length of hospital stay.
• Ulartitide, a synthetic natriuretic peptide currently in Phase III (the TRUE-AHF trial; NCT01661634) or the 4th-generation calcium-channel blocker clevidipine which have been aimed at treating patients with acute heart failure and systolic blood pressure greater than 160 mm Hg.
• The COoperative North Scandinavian ENalapril SUrvival Study (CONSENSUS) investigated the effect of adding enalapril 40 mg to HF management and enrolled 253 patients with severe heart failure. Enalapril benefited symptoms and improved survival with placebo, but had no impact on sudden cardiac death.
• The Studies Of Left Ventricular Dysfunction–Treatment (SOLVDTreatment) randomized 2569 patients with NYHA class II to III heart failure and EF <35% to enalapril 20 mg or placebo. Enalapril group had 16% fewer deaths compared to control arm (P=0.0036), with majority of deaths resulting from progressive heart failure, and 26% fewer hospitalizations (P<0.0001).