Acute myocardial infarction occurring after hypertrophic obstructive cardiomyopathy with paroxysmal atrial fibrillation: a case report

Abstract

Atheromatous plaque rupture and coronary artery stenosis/occlusion are leading causes of acute myocardial infarction (AMI). Other reasons for AMI are frequently overlooked. We report a rare case of AMI occurring after hypertrophic obstructive cardiomyopathy with paroxysmal atrial fibrillation. Although the patient showed multiple lead ST-T changes on an electrocardiogram and elevated circulating cardiac troponin I concentrations, no stenotic lesions were observed by repeated invasive coronary angiography examinations. Hypertrophic obstructive cardiomyopathy with paroxysmal atrial fibrillation was suspected as the primary cause of AMI. The patient received radiofrequency catheter ablation therapy and was free of atrial fibrillation and myocardial infarction 1 year postoperatively. The clinical management and outcome of the patient are also discussed.

Introduction

Hypertrophic cardiomyopathy (HCM) is one of the most common genetic cardiovascular diseases, and is frequently associated with heart failure, sudden cardiac death, and ischemic stroke. ¹ HCM is characterized by a maximal end-diastolic left ventricular wall thickness of ≥15 mm, excluding other causes of myocardial hypertrophy.^2,3 Hypertrophic obstructive cardiomyopathy (HOCM) refers to patients with HCM and a left ventricular outflow tract pressure gradient of ≥30 mmHg. ⁴ Atrial fibrillation (AF) is a prevalent arrhythmia in patients with HCM, and is closely associated with symptom exacerbation, heart failure, thromboembolic events, and an unfavorable prognosis. ⁵ An AF attack can exacerbate myocardial ischemia of HOCM, which may lead to considerable hemodynamic impairment and an increased risk of mortality. ⁶ However, AF is not well controlled by amiodarone in HOCM. ⁷

Clinically, when patients suffer from acute myocardial infarction (AMI) with symptoms, such as ST-T changes in an electrocardiogram (ECG) and elevated circulating concentrations of cardiac enzymes, atheromatous plaque rupture and coronary artery stenosis/occlusion are considered as the primary causes of AMI. However, other possible reasons for this condition are usually ignored. In this report, we described a rare case of AMI. Repeated coronary angiography showed no coronary artery abnormalities in the patient, and we believed that HOCM with paroxysmal AF was likely to be the actual cause of the AMI. We summarize our experience of diagnosis and clinical management of this patient.

Case report

A 66-year-old woman presented to the Emergency Department of our hospital with the complaints of chest pain and chest distress. She also suffered from radiating pain from the left shoulder, shortness of breath, and diaphoresis. She had a history of hypertension and diabetes for 2 years. She did not have a family history of heart disease. Two years previously, this patient had chest pain and chest distress during rest. She presented to the local hospital and was diagnosed with AMI. However, coronary angiography suggested no apparent stenosis in her coronary artery, and she did not receive further investigations or treatment (Table 1).

Table 1.

Timeline of the patient’s course.

Time	Events
2 years previously	The patient presented to a local hospital with chest discomfort at rest. She was diagnosed with AMI, but an invasive coronary angiogram showed no stenosis in her coronary artery.
21 hours before this visit	The patient presented to the local hospital again with symptoms of AMI. She was diagnosed with AMI and AF, and was treated with aspirin, clopidogrel, heparin, irbesartan, and metoprolol.
Admission to our hospital
Day 1	The patient presented to our Emergency Department and was diagnosed with AMI and AF. An invasive coronary angiogram was performed, but showed no apparent abnormalities.
Day 2	The patient had recurrent AF and presented with symptoms of AMI, which ceased spontaneously after a few minutes. She started treatment with amiodarone and enoxaparin.
Day 3	Recurrent AF lasted a few tens of seconds captured on a cardiac monitor, although amiodarone was continued.
Day 5	Echocardiography showed HOCM.
Day 6	We speculated that HOCM with paroxysmal AF may be the mechanism of the AMI.
Day 8	We performed RFCA to control and prevent the patient’s AF.
Day 12	The patient recovered well and was discharged home.
Followed up at 1 year	No recurrent AF or AMI

AMI, acute myocardial infarction; AF, atrial fibrillation; HOCM, hypertrophic obstructive cardiomyopathy.

Twenty-one hours before this visit, she re-experienced chest pain and distress, concurrent with radiating pain in the left shoulder, dyspnea, and diaphoresis. She presented to the local hospital again. An ECG showed AF with a rapid ventricular rate, ST-segment depression in multiple leads, and ST-segment elevation in the AVR lead (Figure 1). The troponin I concentration was elevated to 22.93 ng/mL (reference concentrations, 0-0.02 ng/mL), supporting the diagnosis of AMI and AF. She was treated with aspirin, clopidogrel, heparin, irbesartan, and metoprolol. Her symptoms gradually attenuated. However, 2 hours before this visit, she suffered from chest pain and chest distress again. She visited our Emergency Department, and an ECG showed sinus rhythm, high left ventricular voltage, and ST-segment depression in multiple leads. Troponin and creatinine kinase-MB concentrations were elevated. Therefore, she was initially diagnosed with AMI, paroxysmal AF, and left ventricular hypertrophy. Invasive coronary angiography was then immediately performed. However, the coronary angiography only showed 20% to 30% stenosis in the middle segments of the left anterior descending coronary artery. No stenosis was observed in the left main coronary artery, left circumflex artery, or right coronary artery (Figure 2). The patient then returned to the ward. Two days after the angiography, she had recurrent AF with a rapid ventricular rate. She experienced chest pain, chest distress, and diaphoresis. We found that the ECG ST-segment changes were more obvious when AF relapsed (Figure 1). AF ceased spontaneously after a few minutes, and she was treated with oral amiodarone 200 mg three times a day to prevent AF and enoxaparin 4000 aXa IU every 12 hours for anticoagulation. However, her AF relapsed and lasted a few tens of seconds, and it was captured on a cardiac monitor during hospitalization. However, amiodarone therapy was continued. A physical examination showed little rales in the right lower lobe anteriorly. We discovered a systolic ejection murmur in the third and fourth intercostal spaces at the left margin of the sternum and apex area of the heart, and this was enhanced when the patient performed the Valsalva maneuver. Her troponin I and creatinine kinase-MB concentrations were 7.90 ng/mL (reference, 0–0.02 ng/mL) and 106.00 ng/mL (reference, 0–7.2 ng/mL), respectively. The N-terminal pro-B-type natriuretic peptide concentration was 4360 pg/mL (reference, 0–125 pg/mL). An echocardiographic examination indicated HOCM in this patient, as shown by an increased interventricular septal thickness (19 mm, reference: 6–12 mm) and increased left ventricular posterior wall thickness (16 mm, reference: 6–12 mm). During systole, the blood flow velocity in the left ventricular outflow tract was greatly increased, at approximately 366 cm/s, and the peak pressure gradient was 54 mmHg. The left ventricular ejection fraction was preserved at 64% (Figure 3). In addition, echocardiography showed that her left ventricular wall motion was weakened and uncoordinated.

Figure 1.

Dynamic changes in an electrocardiogram of the patient from symptom onset to recovery after RFCA.

Figure 2.

Coronary angiographic images. (a) A spider view offers visualization of patency of the left main artery and the proximal segments of the left anterior descending artery and the left circumflex artery. (b) The right anterior oblique cranial view shows 20% to 30% stenosis in the middle segments of the left anterior descending artery and (c) Right coronary angiography in the left anterior oblique view shows no stenosis in the right coronary artery.

Figure 3.

Echocardiographic images. (a) Echocardiography in the parasternal long axis view shows asymmetric IVS hypertrophy in end-systole phase. (b) Echocardiography in the parasternal long axis view shows maximal IVSd (c and d). During systole, blood flow velocity (vel) in the left ventricular outflow tract and the peak pressure gradient (PG) were measured and (e) Cardiac parameters derived from an echocardiographic examination.

On the basis of the above-mentioned findings, we considered that her chest pain and distress might have resulted from HOCM. Moreover, the AF attack prominently exacerbated the myocardial ischemia and resulted in AMI. Therefore, we performed transcatheter ablation for pulmonary vein isolation to control her AF. We punctured the left femoral vein using the Seldinger technique and inserted an electrode into the coronary sinus. We punctured the right femoral vein using the Seldinger technique, punctured the atrial septum, and inserted a mapping catheter and an ablation catheter into the left atrium. Under the guidance of a three-dimensional mapping system, we reconstructed the left atrium in three dimensions. Finally, we performed pulmonary vein isolation (Figure 4). After radiofrequency catheter ablation (RFCA), the patient's symptoms were gradually relieved. The troponin I concentration was slightly elevated after the procedure, but was decreased later, which suggested that her AMI was alleviated (Figure 5). The patient recovered well and was discharged home. Oral drugs provided at discharge included amiodarone 100 mg daily, rivaroxaban 100 mg daily, metoprolol 47.5 mg daily, spironolactone 20 mg daily, furosemide 20 mg daily, and dapagliflozin 10 mg.

Figure 4.

Pulmonary vein isolation was performed by three-dimensional reconstruction. Different perspectives are shown in posteroanterior (a), left lateral (b), right anterior oblique (c), and left anterior oblique (d) views. The black arrow indicates the left atrial appendage.

Figure 5.

The patient's serum high-sensitive troponin I concentration greatly increased during an atrial fibrillation attack and then decreased. Recurrent atrial fibrillation during hospitalization only lasted for tens of seconds. Therefore, there was no substantial increase in troponin concentrations. Troponin concentrations slightly increased after RFCA, but finally decreased.

During follow-up 2 months later, she was asymptomatic and had no apparent abnormalities on an ECG (Figure 1). She recovered well and had no apparent chest discomfort in a follow-up 1 year later. During a telephone follow-up, the patient expressed satisfaction with her outcome. The major events of this patient from symptom onset to discharge are shown in a timeline (Table 1). The case report section was written by following the CARE guidelines. ⁸

Discussion

According to the available coronary angiography information over the years, there is a consensus that coronary artery stenosis and atheromatous plaque progression are the primary cause of AMI.^9,10 Therefore, an emergency coronary angiography examination is one of the gold standard approaches for diagnosing AMI. Notably, some patients with AMI do not show apparent coronary abnormalities by an invasive angiography examination. In this case, the patient had AMI 2 years previously. However, the primary physicians in the local hospital ignored further investigations because of the normal angiographic imaging. As a consequence, the patient recurrently suffered from AMI. Because ST-segment changes are poorly specific to epicardial coronary artery disease in patients with HOCM, ¹¹ further tests, including Holter monitoring, echocardiography, and cardiac magnetic resonance, are recommended to determine the actual cause of AMI.

Left ventricular outflow tract obstruction is a common condition of HCM and typically manifests as chest pain, palpitations, dyspnea, and syncope.^2,4 Myocardial ischemia is closely associated with HOCM. However, in clinical practice, differentiating chest pain of HOCM from angina of coronary atherosclerotic heart disease is difficult. ¹² In this patient, paroxysmal AF with HOCM was considered the primary cause of the AMI. We speculate that left ventricular outflow tract obstruction and coronary squeezing were likely to be the mechanism responsible for the myocardial ischemia and the patient's chest pain. Mathew et al. reported 166 patients who received coronary revascularization and required septal myectomy to relieve symptoms due to HOCM. ¹³ Therefore, except for atherosclerotic plaques, other causes of AMI should not be ignored. Although HOCM is infrequent, it could be the root cause of a patient’s discomfort and repeated misdiagnosis if not taken seriously.

AF attacks that lead to hemodynamic disorders can exacerbate the myocardial ischemia of HOCM. AF is a common comorbidity of patients with HCM. ⁵ AF in patients with HCM is associated with a 1.7 times increased risk of sudden cardiac death, 7.0 times increased risk of thromboembolism, 2.8 times increased risk of heart failure, and 2.5 times increased risk of all-cause mortality. ¹⁴ In HCM, the mechanism of myocardial infarction induced by AF is unclear. The possible mechanisms of this condition are as follows.^15,16 (1) Increased wall thickness and left ventricular outflow tract obstruction increase the demand for blood supply in HCM. (2) In patients with HCM, the myocardial perfusion reserve is impaired, especially in the endocardium, which increases with myocardial hypertrophy. (3) Patients with HCM often have microvascular dysfunction manifested by an impaired vasodilator response, which is exacerbated by the degree of hypertrophy. AF may induce ischemic myocardial injury and, in severe cases, induce myocardial infarction by exacerbating the imbalance of blood supply and demand in a hypertrophic heart with impaired myocardial perfusion reserve. Therefore, aggressive treatment of AF in patients with HCM is necessary. However, antiarrhythmic drugs appear ineffective in AF in many patients with HCM. ⁷ In our case of HOCM, recurrent AF was associated with AMI, despite continued amiodarone treatment.

RFCA can decrease atrial arrhythmia and thromboembolic events, maintain long-term sinus rhythm, and improve the quality of life in patients with HCM complicated by paroxysmal AF.^17–21 Therefore, RFCA may be an effective therapeutic strategy for patients with symptomatic drug-refractory AF. Our patient was admitted to our hospital with a diagnosis of AMI in a critical condition. Therefore, we did not perform cardiac magnetic resonance imaging. Consequently, there is no direct evidence of the myocardial infarct area and size, which is a limitation of this report. Notably, after the AF was controlled by RFCA, the patient's symptoms were alleviated, myocardial injury markers were decreased, and there was no recurrent AMI during follow-up, which support our diagnosis. However, the patient continued to receive oral amiodarone treatment. Whether AF will recur when amiodarone treatment is withdrawn is unclear. During the follow-up, the patient was satisfied with the treatment effect. She is presently in good condition, and we will continue to monitor her condition in the future.

In conclusion, coronary artery stenosis and atheromatous plaque progression are the primary cause of acute coronary events. Therefore, an emergency coronary angiogram is necessary for patients with AMI. However, causes other than coronary anomalies should not be ignored. Further tests, such as Holter ECG and echocardiography, should be recommended to identify the cause of AMI, especially for patients who do not have apparent abnormalities in invasive coronary angiography. HOCM with AF is likely one reason for AMI without coronary artery stenosis or occlusion. RFCA should be considered when there is symptomatic HOCM with drug-refractory AF.

Supplemental Material

sj-pdf-1-imr-10.1177_03000605221133702 - Supplemental material for Acute myocardial infarction occurring after hypertrophic obstructive cardiomyopathy with paroxysmal atrial fibrillation: a case report

Supplemental material, sj-pdf-1-imr-10.1177_03000605221133702 for Acute myocardial infarction occurring after hypertrophic obstructive cardiomyopathy with paroxysmal atrial fibrillation: a case report by Dingfeng Fang, Jiabin Xu, Bo Bai and Haibo Chen in Journal of International Medical Research