Holiday heart syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Aditya Ganti M.B.B.S. [3] Apeksha Gupta, MBBS[4]

Overview

Holiday heart syndrome is a clinical presentation of irregular heartbeat pattern, in individuals who are otherwise healthy. It can be the result of stress, dehydration, and drinking. The most common cause of this syndrome is excessive alcohol consumption. Usually associated with binge drinking, it has also been documented in patients who are not heavy alcohol drinkers. The pathophysiology of holiday heart syndrome, or alcohol-induced arrhythmia, is complex, and therefore not completely understood. The most commonly accepted therapy is that chronic ethanol use in large quantities, leads to cardiac structural and cellular changes through a buildup of ethanol and its metabolites. The incidence and prevalence of holiday heart syndrome is unclear due to conflicting evidence. Left untreated, it may culminate in severe cardiomyopathy, valvular disease, and ultimately death. Some patients may develop end-stage liver disease which also has a poor prognosis. If diagnosed early and treated with measures such as alcohol cessation, the prognosis for holiday heart disease is good, as the disease is reversible. Patients with acute exposure to alcohol can present with a variety of symptoms. Holiday heart syndrome is also known as alcohol-induced atrial fibrillation. The finding on physical examination are characteristic, patients show features of alcohol intoxication and their breath smells of alcohol. There could be changes in the mental status, as the person is intoxicated and sometimes hypotensive. Depending on the cardiac rhythm, the patient may have an irregular or thready pulse. Complete blood count may show macrocytic anemia via an elevated mean corpuscular volume. Sometimes an elevated white blood cell count may be seen as alcoholics have decreased immunity and tend to get sick more often. Complete metabolic panel may show 2:1 aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio. Twelve-lead electrocardiography (ECG) is essential to exclude other cardiac pathologies like ischemia, infarction, pulmonary embolism, or hypertrophy. A chest x-ray may show cardiomegaly. An echocardiogram should be performed to evaluate for any structural abnormalities and to assess the cardiac status and function. Echocardiography is the standard diagnostic method for assessment of cardiac chamber enlargement, left ventricular (LV) wall motion abnormalities, hypertrophy, valvular disease, and both systolic and diastolic dysfunction.The mainstay of treatment for holiday heart syndrome depends on the patients vitals at the time of presentation. For unstable patients with atrial fibrillation, cardioversion is the recommended treatment. If the patient is stable, the therapeutic indication is for arrhythmia treatment.

Historical Perspective

• Holiday Heart Syndrome was first identified back in 1978 (Ettinger et al) who conducted a study on subjects who regularly consumed heavy quantities of alcohol and also took part in a drinking binge prior to the study evaluation.The term was thus coined by Ettinger et al in 1978.

Pathophysiology

• The pathophysiology of holiday heart syndrome, or alcohol-induced arrhythmia, is complex, and thus remains unresolved
• It may be due to the direct myotoxic effects of alcohol or the indirect effects caused by its metabolism.

There are several mechanisms believed to be the causative factor of holiday heart syndrome :

• The most accepted theory is that chronic ethanol consumption in large quantity, leads to cardiac structural and cellular changes through the accumulation of ethanol and its metabolites.
• It causes oxidative stress to the myocardium by increasing the generation of free radicals and activating the Renin Angiotensin system.
• These metabolites cause oxidative damage, mitochondrial dysfunction, cell death, lower the effects of cardio-protective molecules, alter protein synthesis and impair calcium transport.
• The most common metabolite responsible for these changes is acetaldehyde, which is produced by the liver by a chemical reaction with alcohol dehydrogenase.
• Acetaldehyde is a major factor responsible for apoptosis which leads to myocytes loss and adverse remodeling .
• Another factor responsible in an altered fatty acid metabolism.
• It is believed to cause arrhythmias by increasing the systemic and intra-myocardial catecholamines (epinephrine and norepinephrine), thus causing the imbalance in the autonomic nervous system.
• It also causes the activation of the Parasympathetic Nervous System, thus causing increased vagal tone and slowing the refractory period of atrium . This high risk of electrical disturbance in the Holiday heart syndrome, is just like dilated cardiomyopathy.
• On a microscopic level, findings in alcoholic cardiomyopathy are indistinguishable and similar to the findings in dilated cardiomyopathy.
• The structure of the mitochondrial reticulum in the myocytes is grossly altered.
• The most common arrhythmia seen in patients with Holiday heart syndrome is Atrial fibrillation, followed by atrial flutter and premature ventricular contractions .

Causes

• The most common cause of holiday heart syndrome is excessive alcohol consumption. The risk is further accentuated by binge drinking episodes by people who already have a chronic drinking background . So on the whole it is a combination of trigger factors like :

• Drinking too much alcohol or caffeine
• Overeating
• Fatigue
• Stress
• Dehydration

Differentiating Holiday Heart Syndrome from Other Diseases

Holiday heart syndrome must be differentiated from

• Alcoholism
• Arrhythmia like Paroxysmal Supra-ventricular Tachycardia
• Atrial fibrillation
• Atrial flutter
• Cirrhotic cardiomyopathy
• Dilated cardiomyopathy
• Psychiatric problems
• Hyperthyroidism and Thyrotoxicosis
• Pulmonary embolism

Disorders	Etiology	Clinical Presentation	Laboratory findings	Electrocardiogram	Echocardiography
Atrial Fibrillation	Elderly Following bypass surgery Mitral valve disease Hyperthyroidism Diabetes Heart failure Ischemic heart disease Chronic kidney disease Heavy alcohol use Left chamber enlargement	General fatigue Rapid and irregular heartbeat Fluttering in the chest Dizziness Shortness of breath and anxiety Fainting Sweating Chest pain	Renal function and electrolytes are routinely determined. Thyroid function tests : Thyroid-stimulating hormone (TSH) is commonly suppressed in hyperthyroidism and of relevance if amiodarone is administered for treatment. Complete blood count Cardiac markers : In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be commenced.	Irregularly irregular rhythm Absent P wave Fibrillatory waves PR interval absent QRS interval less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction	Valvular heart disease Left and right atrial size LV size and function Peak RV pressure pulmonary hypertension LV hypertrophy LA thrombus (low sensitivity) Pericardial disease
Atrial Flutter	Elderly Alcohol	Shortness of breath Chest pain Lightheadedness or dizziness Nausea and, in some patients, nervousness and feelings of impending doom Anxiety Weakness Syncope	Complete blood count is routinely done to look for anemia Differential count to look for elevated white cell count in infectious causes like pericarditis Thyroid function tests are done to look for hyperthyroidism, which is a potential cause of atrial flutter Blood gas analysis is done to look for hypoxia and carbon monoxide poisoning Erythrocyte sedimentation rate Urinalysis Liver function tests Pre-warfarin coagulation screen(INR/aPTT)	Irregular or regular rhythm Sawtooth pattern of P waves at 250 to 350 bpm Biphasic deflection in V1 PR interval varies QRS interval less than 0.12 seconds, consistent, and normal in morphology	Detection of left atrial appendage and right atrial appendage thrombi Estimation of blood flow velocity in the left or right atrium and left and right atrial appendage Detection of right atrial and right atrial appendage thrombi Regular undulatory waves of the posterior left atrial wall Regular undulatory waves of the upper left interventricular septum
Cirrhotic cardiomyopathy	Cirrhosis Chronic liver failure	Dizziness Dyspnea on exertion Chest pain Heart palpitations Weakness Angina	Complete metabolic profile Liver function tests Urinalysis Renal function and electrolytes are routinely determined Coagulation studies (INR/aPTT) are usually performed	QT interval prolongation, Electrical dyssynchrony	Dilated left atrium, Thick LV walls, Systolic and/or diastolic dysfunction
Paroxysmal Supraventricular Tachycardia	Alcohol Caffeine Nicotine Psychological stress Wolff-Parkinson-White syndrome Heart failure Thyroid disease Chronic lung disease Drugs like cocaine and methamphetamine Asthma medications and over-the-counter cold and allergy drugs	Palpitations Shortness of breath Dizziness Sweating A pounding sensation in the neck Syncope	Electrolytes like Na+, K+, and Ca2+ -electrolyte abnormalities is a major factor for paroxysmal supraventricular tachycardia Thyroid function tests are done to look for hyperthyroidism, which is a potential cause of paroxysmal supraventricular tachycardia Complete blood count	Regular rhythm P wave absent or hidden in QRS PR interval absent Narrow complexes (< 0.12 s)	To assess for any evidence of significant underlying structural heart disease
Dilated Cardiomyopathy	Idiopathic Myocarditis Substance abuse Connective tissue disease Nutritional deficiencies Infiltrative diseases Toxins.	Lateral displacement of the point of maximal impulse Right ventricular heave S2 at the base S3 gallops Jugular venous distension Peripheral edema	Detecting the cause (such as thyroid function tests, toxicology screening, and genetic counselling) Assessing the cardiac complications of the condition	Left ventricular hypertrophy Atrial fibrillation or premature ventricular complexes Conduction delays, AV nodal block, or left bundle branch block	Ventricular and atrial dilatation Increased left ventricular mass Global reduction in systolic function Focal wall motion abnormalities
Hyperthyroidism	Primary: Grave's disease, toxic thyroid nodules and adenoma Secondary: Pituitary adenomas and intracranial tumors Tertiary:Intracranial tumors involving the hypothalamus	Goiter Palpitations Anxiety Heat intolerance Weight loss Diarrhea Exophthalmus	Elevated T3 and T4 hormones TSH: Reduced in 1ry and Elevated in 2ry hyperthyroidism. Thyroid stimulating antibodies: Elevated only in Grave's disease	Sinus tachycardia Atrial fibrillation High left-ventricular voltage	The following may be present: Left ventricular enhanced systolic function Enhanced or impaired diastolic function Heart failure with preserved ejection fraction
Pulmonary Embolism	Surgery Prolonged immobilization Fractures or Trauma Oral contraceptives or supplemental estrogen Pregnancy Overweight Smoking Hyper coagulable states Heart failure Cancer	Tachypnoea Tachycardia Fever Chest pain Hemoptysis Excessive sweating Lightheadedness or dizziness	Blood tests: D-dimer blood test Troponin BNP: Brain natriuretic peptide On CT angiography: Intra-luminal filling defect On MRI: Narrowing of involved vessel No contrast seen distal to obstruction Polo-mint sign (partial filling defect surrounded by contrast)	S1Q3T3 pattern representing acute right heart strain	Direct visualization of Thrombi in Right atrium or Pulmonary artery Right ventricular dilatation Right ventricular dysfunction Pulmonary artery dilatation Normal or hyper-dynamic Left ventricle
Alcoholism	Acute or chronic alcohol intake	Loss of coordination, Flushing of the face. Speech abnormalities like slurred speech. Damp or clammy skin. Mood swings Aggression or depression. Drowsiness.	Blood alcohol content (BAC). Macrocytosis (enlarged MCV) Elevated GGT Moderate elevation of AST and ALT and an AST: ALT ratio of 2:1. High carbohydrate deficient transferrin (CDT)	P-wave and QTc prolongation, T-wave abnormalities QRS complex prolongation.	To assess for any evidence of significant underlying structural heart disease

Epidemiology and Demographics

• The incidence and prevalence of holiday heart syndrome is unclear due to conflicting evidence. It is a common presentation in the emergency room, around 35-62% of atrial fibrillation cases precipitated by alcohol drinking.

Natural History, Complications, and Prognosis

Natural History

• If left untreated, it may culminate in severe cardiomyopathy, valvular disease, and ultimately death. Some patients may develop end-stage liver disease which also has a poor prognosis.

Complications

• Complications of the holiday heart syndrome include:
  • New or worsening heart failure
  • Life-threatening arrhythmias
  • Community-acquired pneumonia
  • Thromboembolism
  • Death

Prognosis

• The overall prognosis of Holiday Heart Syndrome depends on the presence of any underlying heart disease.

• If diagnosed early and treated with alcohol cessation, the prognosis for holiday heart disease is good as the disease is reversible.

Diagnosis

History and Symptoms

• The attacks occur more frequently either in the early morning or late at night, but have also been reported during daytime.
• Patients often give a history of heavy alcohol intake prior to the episode.
• A history of alcoholism should alert physicians to concomitant illnesses such as alcohol-related cardiomyopathy and chronic liver disease.

Symptoms

Patients suffering from Holiday heart Syndrome suffer from the following symptoms:

• Dizziness
• Dyspnea on exertion
• Chest pain
• Unconsciousness
• Heart palpitations.
  • Palpitations are the most common symptom when a patient presents to the hospital for atrial fibrillation.
  • These can be intermittent or persistent, depending on the presence or absence of a sustained arrhythmia and the ventricular response to atrial fibrillation.
• Fatigue
• Weakness
• Angina
• Other signs of alcohol intoxication. Patients with acute exposure to alcohol can present with a variety of symptoms.The most common symptoms are :
  • palpitations during exertion
  • reduced physical ability
  • palpitations at rest
  • shortage of breath during exertion
  • anxiety

• Some patients can also have uncommon symptoms like:
  • Swollen legs
  • Nausea
  • Anxiety

Physical Examination

• On physical examination, there may be a strong evidence of alcohol intoxication and strong odor of alcohol in their breath.

• Depending on the cardiac rhythm, the patient may have an irregular or thready pulse.
• Presence of an "irregularly irregular" pulse.
• Protodiastolic (S3), and Presystolic (S4) heart sounds may be heard.
• Hypotension
• In advanced cases, signs of right heart failure like jugular venous distention, ascites, and peripheral edema are seen.

Laboratory Findings

• The following laboratory findings can help in diagnosis of holiday heart syndrome.
  • Complete blood count may show macrocytosis via an elevated mean corpuscular volume and increase in hemoglobin
  • Thrombocytopenia
  • Elevated white blood cell count may be seen
  • Complete metabolic panel may show 2:1 aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio, suggestive of alcoholic liver disease
  • Increased serum levels of gamma-glutamyl transpeptidase.
  • Magnesium and thiamine are commonly low in alcoholics.
  • Urine tests also exist including ethyl glucuronide and ethyl sulfate , which are both biomarkers signifying the breakdown of alcohol.
  • Gamma-glutamyl transferase may be high in these patients.
  • Another blood test to identify alcohol use is phosphatidyl ethanol (PEth), a marker.
  • This is typically measured in blood and can indicate moderate to heavy drinking.
  • Carbohydrate-deficient transferrin is useful to identify patients who have relapsed following a period of abstinence.

• Twelve-lead electrocardiography (ECG) is essential to exclude other cardiac pathology such as ischemia, infarction, pulmonary embolism, or hypertrophy.
• ECG may show arrhythmias like atrial fibrillation [AF], QT interval prolongation, increased QRS duration and conduction abnormalities like left bundle branch block
• A chest x-ray may show cardiomegaly
• Echocardiography, performed to evaluate for any structural abnormalities and to assess cardiac function, is the standard of care for assessment of cardiac chamber enlargement, left ventricular (LV) wall motion abnormalities, hypertrophy, valvular disease, and both systolic and diastolic dysfunction.
• Liver disease is often a feature holiday heart syndrome as alcohol damages the liver. Therefore, ultrasound of the liver may reveal liver cirrhosis.

Treatment

Usually the symptoms associated with holiday heart syndrome, that is atrial fibrillation and other conduction abnormalities, dissipate with appropriate rest, hydration and no additional treatment within 6 to 12 hours, once alcohol intake is stopped. But if they persist longer or the symptoms get severe, medical attention is required.The mainstay of treatment for holiday heart syndrome depends on the patients vitals at the time of presentation. The patient will be attached to a heart monitor to evaluate the rhythm of the heart and confirm the diagnosis.The mainstay of treatment for holiday heart syndrome depends on the patients vitals at the time of presentation.

• If the patient presents with atrial fibrillation, an IV line is started for hydration and depending on the heart rate, medication is administered to slow the heart rate.

• If the patient is unstable and has atrial fibrillation, cardioversion is the recommendation.
• If the patient is stable, the therapeutic indication is for arrhythmia treatment.
  • Complete alcohol cessation was needed to see a reversal of the disease process,
  • The patient must be encouraged to join alcoholics anonymous (AA) and other support groups.
• Patients presenting to the emergency department with sustained tachyarrhythmia secondary to acute alcohol toxicity usually can be observed with electrocardiographic monitoring.

Prevention

• On a broader level, the main treatment for alcoholic cardiomyopathy is abstinence from alcohol .
• Replace electrolytes like potassium and others which are lost through urination. Drink sufficient water as dehydration is a major cause of electrolyte imbalances.
• Limit the intake of salt and sugar in diet, as it can raise the blood pressure.
• Control stress, which can increase your heart rate and blood pressure.