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Why is this middle-age patient having recurrent stomach pain and fainting episodes after drinking alcohol? That's the question facing Yunfei Gu, MD, of Luoyang Central Hospital Affiliated to Zhengzhou University in China, and colleagues, who detailed their case study in .

The patient, who was in their 50s, was admitted to the hospital, where symptoms intensified. The individual acknowledged being a smoker and heavy drinker for the last 20 years, with an average alcohol intake of 250 g/week. The symptoms had been ongoing for 2 years.

Hypertension had been diagnosed 3 months prior. Intake assessments revealed a high-sensitivity troponin I of 0.01 ng/mL and serum potassium of 4.6 mEq/L, both in normal range.

Given the upper abdominal pain, dizziness, and fainting, clinicians directed the patient to gastroenterology for assessment. They learned that symptoms were transient, lasting from 5 to 10 minutes, and usually occurred about 6 to 20 hours after drinking. Syncope only developed after the patient had consumed a significant amount of alcohol.

During one of the episodes, clinicians used an ECG to record cardiologic effects. Findings revealed "a high-degree atrioventricular block and premature ventricular contractions. The ST segments in leads II, III and aVF [were] 4 to 6 mm elevated, while the ST segments in leads V₂ through V₆ [were] substantially depressed," the authors wrote.

The second ECG showed "a sinus rhythm with short bursts of ventricular tachycardia, [as well as] widespread ST-segment elevations (4-15 mm) in leads II, III, aVF, and V₂ through V₆."

Based on the ECG findings, the patient was transferred to the cardiology department. There, the team performed coronary angiography, which revealed "only 10% stenosis in the proximal left anterior descending artery (LAD) and right coronary artery (RCA)," and no evidence of stenosis affecting the left main and circumflex coronary artery.

Based on the patient's clinical course, along with the changes on ECG and coronary angiography findings, clinicians suspected alcohol-induced Prinzmetal variant angina. They treated the patient with a calcium antagonist to help reduce the duration of abdominal pain while he was hospitalized.

In addition, they prescribed atorvastatin (Lipitor), aspirin, and clopidogrel (Plavix). "Importantly, the patient stopped smoking and consuming alcohol," Gu and team noted.

The patient was discharged and has not experienced further abdominal pain or episodes of syncope over the course of a 2-year follow-up.

Discussion

" is a type of variant angina with transient ST-segment elevation caused by the spasm of coronary arteries," Gu and colleagues wrote.

Unlike classic angina, which tends to occur with exertion, this variant type generally occurs at rest and may be triggered by various factors including cold, coffee, emotional agitation, and alcohol. Indeed, the authors noted that alcohol has been of cases of variant angina pectoris.

They also cited a recent of over 5,000 Korean patients with typical or atypical chest pain and no significant coronary artery disease, which identified alcohol consumption as a risk factor for coronary artery spasm. Those who consumed alcohol had higher incidence of coronary artery spasm compared with non-drinkers (62% vs 58%, P=0.016), as well as spontaneous spasm (22% vs 17%, P=0.004), multi-vessel spasm (37% vs 31%, P=0.009), proximal epicardial spasm (46% vs 39%, P=0.002), and chest pain (46% vs 42%, P=0.047).

However, the status and pattern of alcohol use had no effect on major adverse cardiac events and recurrent angina requiring repeat coronary angiography at 5 years, the study authors noted.

Gu and colleagues also cited another of a patient with Prinzmetal angina in which "chest pain occurred each time 10 to 11 hours after alcohol ingestion, when blood concentration of alcohol had already decreased to 0, indicating a withdrawal from an acute exposure of alcohol as a possible trigger to coronary spasm."

Despite the poorly understood mechanism behind this variant angina, vascular endothelial dysfunction due to alcohol ingestion has been linked with coronary spasm, they said. "This includes alcohol-induced elevation in plasma endothelin-1 and decrease in plasma prostaglandin F1 alpha and cyclic guanosine monophosphate."

The endothelial dysfunction observed in their own patient may have been due to a long history of smoking and alcohol use, they pointed out. In addition, East Asian populations may be at greater risk of alcohol-induced vasospasm due to the high prevalence of aldehyde dehydrogenase 2 deficiency.

The ECG changes that occur in patients with variant angina are influenced by how long the vessel spasm lasts, and which coronary arteries are involved, they wrote. "Longer spasms of the RCA can lead to inferior myocardial infarction and atrioventricular block while vessel spasm in the LAD may introduce anterior myocardial infarction."

However, spasm affecting any coronary artery can cause malignant ventricular arrhythmias, they added.

That this patient had a single episode associated with transient ST-segment elevation in the inferior leads and concurrent high-degree atrioventricular block suggests that the RCA was involved at that moment, Gu and team wrote. "The other episode with widespread ST-segment elevation in the anterior and inferior leads and simultaneously one burst of nonsustained ventricular tachycardia perhaps involved LAD arteries."

Alcohol cessation is central to management of alcohol-induced Prinzmetal variant angina, they noted. In addition, clinicians may add dual antiplatelet therapy with clopidogrel and aspirin for patients who develop "severe outcomes of cardiovascular events, e.g., ventricular tachycardia and complete atrioventricular block as in the present case," they wrote.

Gu and colleagues urged clinicians to consider Prinzmetal variant angina as a differential diagnosis in patients who develop chest pain within 24 hours of alcohol consumption, adding that prognosis is good for most patients with this alcohol-induced variant angina.

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