Heart failure

• 1. Introduction

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  In 2022, about 64 million people around the world were living with heart failure. The name sounds like an ending, yet the condition is usually a slow struggle. Heart failure, also called congestive heart failure, is a syndrome. The heart has lost some of its ability to fill with blood and push it onward. Around 2% of adults are affected. It is not the same thing as cardiac arrest, where blood flow stops completely. In heart failure the pump keeps running, but not well enough for the body's needs.

  How does a struggling pump announce itself, and why do the lungs and the legs both pay the price? What damages the heart in the first place, and can ordinary medicines be part of the story? How do doctors turn a weak heart into a single percentage? And why is this the leading cause of hospitalization and readmission in older adults?

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• 2. The Backed-Up Body

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  Some doctors ask a patient a very plain question: how many pillows do you need to sleep? The answer is a measurement. Trouble breathing while lying flat is called orthopnea. In extreme cases a person cannot lie down at all and sleeps sitting upright.

  That symptom comes from the left side of the heart, which collects oxygen-rich blood from the lungs and sends it to the rest of the body. When it falters, blood backs up into the lungs. Breathing becomes labored and fatigue sets in, because tissues receive too little oxygen. A doctor listening to the chest may hear crackling sounds, first at the bottom of the lungs and later across all of them. That crackle signals fluid in the tiny air sacs. A bluish tint to the skin is a late sign of extremely severe fluid buildup.

  A sudden attack called paroxysmal nocturnal dyspnea strikes some patients several hours after they fall asleep. Others wheeze in what is called cardiac asthma. When the left side cannot send enough blood forward, the signs spread beyond the lungs. Dizziness, confusion and cool hands and feet can appear at rest, and the brain may be starved enough to cause fainting.

  The right side of the heart tells a different story. It is often undermined by lung problems such as pulmonary hypertension. Fluid collects in the body instead of the lungs. People who stand a lot notice swollen feet and ankles. People who lie down a lot get swelling over the lower back instead. At night, fluid from the legs returns to the bloodstream, which can send a person to the toilet repeatedly. In worse cases the abdomen swells with fluid and the liver enlarges. A congested liver can turn the skin yellow and disturb blood clotting.

  One early clue hides in blood pressure. The gap between the top and bottom numbers, called pulse pressure, is often narrow in heart failure, at 25% or less of the top number. If one ventricle fails for long enough, the other usually follows. When two sides fail together, fluid can also pool between the lung and the chest wall, most often on the right.

  Left-sided failure is the more common form, and it is the right ventricle that pays for it. Raised pressure in the lung vessels adds stress to the right side, and the reverse harm is far milder.

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• 3. How the Pump Fails

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  The Frank-Starling law, named for the physiologists Otto Frank and Ernest Starling, describes a clever rule in a healthy heart. The more the chamber fills, the harder it squeezes, and the more blood it sends out. In heart failure that rule breaks. The chamber is stretched so far that the muscle contracts less efficiently. The reason is that overstretched fibers can no longer link their actin and myosin filaments well.

  Meanwhile the body's own alarm systems make things worse. Long-lasting activation of the renin-angiotensin system and the sympathoadrenal system raises the heart's workload. Over time the left ventricle scars, widens and changes shape, from an elliptical form to a spherical one.

  Because heart failure is a syndrome and not a single disease, finding what triggered it is central to care. The source calls it the potential end stage of all heart diseases. Common causes include coronary artery disease, a previous heart attack, high blood pressure, atrial fibrillation, valve disease, heavy drinking, infection and cardiomyopathy of unknown origin. A viral infection can inflame the heart muscle, a condition called myocarditis, and genes play an important role. When several causes are present together, progression is more likely and the outlook is worse.

  The list of less obvious injuries is long. Systemic viral infections such as HIV can damage the heart. So can the chemotherapy drugs daunorubicin, cyclophosphamide and trastuzumab, along with cocaine and methamphetamine. Exposure to lead or cobalt is a rare cause. Amyloidosis and lupus can also harm the muscle. Obstructive sleep apnea is treated as an independent cause, and recent clinical trial reports link variation in blood pressure to cardiac changes that may lead to failure.

  High-output heart failure turns the usual picture around. Here the heart pumps more than normal and still cannot keep up. Triggers include severe long-term anemia, an overactive thyroid, cirrhosis, Paget's disease, multiple myeloma, abnormal connections between arteries and veins, and beriberi, a deficiency of vitamin B1.

  Even a stable patient can tip over the edge. Pneumonia, a heart attack, an abnormal rhythm or uncontrolled hypertension can set off a sudden decline, which doctors call acute decompensation. So can something as ordinary as neglecting a fluid limit, a diet or a prescribed medicine.

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• 4. Hidden Culprits

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  Nonsteroidal anti-inflammatory drugs, known as NSAIDs, double the risk of heart failure, according to the source. They block the formation of prostaglandins. As a result the body holds on to fluid, blood pressure rises, and diuretics work less well. The American College of Cardiology and the American Heart Association advise against COX-2 inhibitors for people with heart failure.

  Other drugs carry their own dangers. Thiazolidinediones, used for diabetes, have been strongly linked to new cases and to worsening disease, because they bring weight gain and fluid retention. Two calcium channel blockers, verapamil and diltiazem, reduce the force of each heartbeat. They are therefore not recommended when ejection is already reduced. The source also names ketamine, pregabalin, minoxidil, itraconazole, lithium, tamsulosin and salbutamol among drugs that may cause or worsen the disease, along with some antipsychotics, antidepressants and stimulants.

  Cancer treatment brings its own burden. One meta-analysis pooled data from 26 studies covering 836,301 breast cancer patients. Survivors faced a higher risk of heart failure within ten years of diagnosis, with a hazard ratio of 1.21. The pooled rate was 4.44 cases per 1000 person-years of follow-up.

  Herbal products are not harmless either. Aconite can slow the heart and trigger dangerous rhythms. Ginseng can push blood pressure too low or too high and can interfere with diuretics. Gossypol strengthens diuretics until they become toxic, while gynura lowers blood pressure. Licorice does the opposite, raising blood pressure and encouraging fluid retention.

  Lily of the valley acts on the heart in ways similar to digoxin and can slow it. Tetrandrine lowers blood pressure by blocking L-type calcium channels. The last on the list, yohimbine, worsens heart failure by raising blood pressure through its action on alpha-2 adrenergic receptors.

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• 5. Measuring a Failing Heart

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  A normal ejection fraction sits between 50% and 75%. That figure is the share of blood the heart pushes out during one contraction, and it has become the main yardstick for sorting heart failure into types. Below 40% is heart failure with reduced ejection fraction, known as HFrEF. A reading of 41-49% is mildly reduced. In heart failure with preserved ejection fraction, or HFpEF, the squeeze is normal but the ventricle is too stiff to relax and fill. Some patients move back above 50% and are classed as having recovered ejection fraction.

  The measurement usually comes from an echocardiogram, an ultrasound of the heart. It can also show valve disease, the state of the sac around the heart and clues to a recent lack of blood supply. In children, doctors prefer a related measure called the shortening fraction. A carotid ultrasound has even been found useful in men over 60, since stiffer neck arteries signal greater risk.

  Blood tests add another layer. In the United Kingdom, guidelines published in 2018 by the National Institute for Health and Care Excellence favor NT-proBNP, followed by a heart ultrasound if the result is high. European and American societies accept either NT-proBNP or BNP. The test can also separate breathlessness caused by the heart from breathlessness with other causes. Low sodium in the blood is common, because the body retains water faster than it retains salt.

  Other tools fill in the picture. A chest X-ray can show an enlarged heart and telltale lines called Kerley lines. An electrocardiogram is not specific, yet a normal one virtually rules out weak pumping on the left side. Angiography, which injects contrast dye through a catheter, can reveal blocked coronary arteries that might be repaired. After death, tissue from the lungs can show iron-laden cells called siderophages, a sign of chronic left-sided failure.

  Even so, no single test has been agreed as the gold standard, especially for HFpEF. The European Society of Cardiology built a scoring algorithm named HFA-PEFF to help, and a 2021 international report proposed a Universal Definition of Heart Failure.

  Severity is graded separately. The New York Heart Association scale runs from class I, with no limits on activity, to class IV, with symptoms even at rest. It is widely used, though it is not very reproducible and does not reliably predict walking distance. In its 2001 guidelines, the American College of Cardiology and American Heart Association added four stages, A through D. Stage A means high risk with no heart disorder yet, a window where prevention may still work. Stage D means advanced disease needing hospital support, a transplant or palliative care.

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• 6. Layers of Treatment

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  Since 2021, the standard of care for HFrEF has been quadruple therapy. It combines an angiotensin receptor-neprilysin inhibitor, a beta blocker, a mineralocorticoid receptor antagonist and an SGLT2 inhibitor. SGLT2 inhibitors reduce hospitalizations and deaths whether or not a patient has type 2 diabetes. In 2022, American guidelines named the combined drug sacubitril/valsartan as the first choice among drugs that block the renin-angiotensin system. Switching to it requires stopping an ACE inhibitor at least 36 hours earlier.

  Older drugs keep their places. ACE inhibitors improve survival, and angiotensin receptor blockers step in when an ACE inhibitor causes a long-term cough. For people who cannot take either, hydralazine with isosorbide dinitrate reduces deaths, and it is especially beneficial in the black population. Spironolactone and eplerenone add benefit on top of beta blockers. Ivabradine helps those whose resting heart rate stays above 70 beats per minute despite optimal therapy.

  For HFpEF, the source finds no convincing drug treatment. Diuretics such as furosemide relieve congestion, though evidence for them is limited. Digoxin, from the foxglove plant, has a narrow safe range and failed trials to show lasting benefit, so few patients now take it. Treating anemia, including intravenous iron when iron is low, improves quality of life. In a sudden crisis, doctors may give nitroglycerin, furosemide and breathing support. Extra oxygen is advised only when saturation falls below 90%.

  Devices come next. An implantable cardioverter-defibrillator is recommended when ejection fraction drops below 35%. It does not ease symptoms, but it cuts deaths from dangerous rhythms. About one-third of people with that level of weakness have signals that reach the two ventricles out of step. For them, cardiac resynchronization therapy restores a normal sequence and improves symptoms and survival. In the other two-thirds, it may do harm. Cardiac contractility modulation, which sends gentle, non-stimulating electrical signals, won United States approval in 2019.

  For the most severe cases, ventricular assist devices were first used as a bridge to heart transplantation and are now also a destination treatment. A transplant can resolve heart failure, but the recipient must stay on immunosuppressive drugs. The shortage of donor hearts is a major limit. Palliative care is meant to start early rather than as a last resort. A 2016 and 2017 review tied it to better quality of life and greater satisfaction with care.

  Daily habits matter too. Fluid restriction is a cornerstone, although evidence for cutting salt was poor as of 2018. Thirst can be a burden, and chewing gum helps. Exercise should suit each person. Phone calls or text messages as prompts, or a treadmill left in plain sight, make it more likely to happen. Cardiac rehabilitation improves quality of life and lowers hospital admissions, though it has not been shown to lower deaths. Home visits and clinic follow-up reduce hospital stays and improve life expectancy.

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• 7. Risk and Toll

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  In the United States, 5.8 million people live with heart failure, and 550,000 new cases are diagnosed each year. One in five adults at age 40 will develop it during the rest of their lives. About half of those who do are dead within 5 years. In 2011 it was the most common reason for hospital admission among adults aged 85 and older, and the second most common for those aged 65-84.

  The revolving door of readmission is stark. Nearly one in four patients, 24.7%, returns within 30 days, and more than half within six months. The average stay is six days. In 2011, readmissions ran at 30.4 per 100 admissions for Medicaid patients and 16.8 per 100 for the uninsured. Both were the highest rates for their groups. Privately insured patients did not have heart failure among their top ten causes of 30-day readmission.

  The odds of survival shift with time. In the first year after diagnosis, about 35% of patients die. In the second year, the risk falls below 10% among those still alive. Later, progressive disease carries an annual death rate near 10%. Strokes follow too: about 18 of every 1000 patients suffer one in the first year, rising to nearly 50 per 1000 by five years.

  In the United Kingdom, heart failure accounts for 5% of emergency hospital admissions. Its overall rates are similar to those of breast, lung, prostate and colon cancer added together. People from deprived backgrounds tend to be diagnosed at a younger age.

  In tropical countries, valve disease and cardiomyopathy are the most common causes. As poorer countries grow wealthier, diabetes, hypertension and obesity rise, and heart failure follows. Men develop heart failure more often, yet total prevalence is similar in both sexes because women live longer with it. Women are older at diagnosis and more likely to have the stiff-ventricle form. In the United States, higher rates among African Americans, Hispanics, Native Americans and recent Eastern European immigrants are linked to diabetes and hypertension. Sources disagree about whether people of Asian descent face higher risk.

  Rates are expected to climb, mainly because people live longer. Risk factors such as hypertension, diabetes, abnormal blood fats and obesity are rising too. Better survival after heart attacks, valve disease and rhythm disorders also leaves more people alive to develop heart failure.

  Prevention has real leverage in the numbers, though. People who reach 500 MET-minutes of exercise a week, the minimum in United States guidelines, have lower risk than those who do not exercise in their free time. Controlling blood pressure and cholesterol matters, and so does avoiding tobacco. Diabetes is a major risk factor. In women with coronary heart disease, it was the strongest one. Women without diabetes or other risk factors have an annual incidence of 0.4%. For diabetic women with a high body mass index, the figure was 7%, and for those with weakened kidney clearance it was 13%.

  The bill is enormous. In 2011, nonhypertensive heart failure ranked among the ten costliest conditions for hospital stays in the United States, with hospital costs above 10.5 billion dollars. The total American cost exceeds 35 billion dollars, and in the United Kingdom it is estimated at 2% of the National Health Service budget. Most of that spending comes from hospitalizations.

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• 8. The Long Road to Understanding

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  The Ebers papyrus, written down around 1550 BCE, holds what may be the first documented observations of heart failure. Egyptians relieved fluid buildup and shortness of breath by bloodletting. The old name for the problem was dropsy, a general term for swelling that covered many cases of what is now called heart failure, along with other illnesses. Greek writers described breathlessness, fluid retention and fatigue that fit the picture. Romans treated dropsy with sea squill, a flowering plant containing cardiac glycosides. India and China left descriptions too, but each culture read the symptoms through its own medical theory.

  Understanding sharpened slowly. Avicenna linked breathlessness to heart disease around 1000 CE. In the 13th century Ibn al-Nafis described the circulation through the lungs, and in 1628 William Harvey described circulation through the body. By the 17th and 18th centuries, doctors joined swelling and breathlessness into one concept. Richard Lower linked shortness of breath with foot swelling in 1679. Giovanni Maria Lancisi tied distended neck veins to right ventricular failure in 1728. In the 19th century, dropsy from kidney failure was told apart from dropsy of the heart.

  New instruments widened the view. René Laennec invented the stethoscope in 1819. Wilhelm Röntgen discovered X-rays in 1895, and Willem Einthoven described electrocardiography in 1903. In 1954, Inge Edler and Hellmuth Hertz invented echocardiography, opening a new era of evaluation.

  Treatments evolved in parallel. Bloodletting, even with leeches, lasted for centuries. In 1749 Jean-Baptiste de Sénac recommended opiates for acute breathlessness. Then, in 1785, William Withering described the foxglove plant's use against swelling. Its extract holds digoxin, still used today. Paracelsus noted the diuretic effect of inorganic mercury salts in the 16th century, and in the 19th century physicians such as John Blackall and William Stokes used them. In 1877 the English physician Reginald Southey invented small tubes to drain fluid directly from swollen limbs. Organic mercury diuretics arrived in 1920. Oral versions and thiazide diuretics followed in the 1950s, and loop diuretics joined in the 1960s. That decade also saw Christiaan Barnard perform the first heart transplant, on a patient with heart failure.

  Research continues in two directions. Some work on stem cells shows tentative evidence of longer life and better ejection fraction after treatment with cells from bone marrow, though other studies show no benefit. A growing body of work looks at epigenetic processes, including DNA methylation and chemical changes to histones, as drivers of cardiac hypertrophy and fibrotic scarring.

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