A 66-year-old female presented to the emergency room with an episode of chest pain that lasted for a few minutes before resolving spontaneously. Electrocardiogram showed a left bundle branch block, left ventricular hypertrophy, and T wave inversions in the lateral leads. Initial cardiac troponin level was 0.15 ng/ml, with levels of 4 ng/ml and 9 ng/ml obtained 6 and 12 hours later, respectively. The peak blood pressure recorded was 195/43 mmHg. Echocardiogram with DEFINITY showed a small left ventricular cavity with apical hypertrophy, and coronary angiogram showed no stenotic or occluding lesions in the coronary arteries. The patient was admitted for a type 2 myocardial infarction with hypertensive crises. She was diagnosed with having apical hypertrophic cardiomyopathy, which is a variant of hypertrophic cardiomyopathy (HCM) in which the hypertrophy predominantly involves the apex of the left ventricle resulting in midventricular obstruction, as opposed to the left ventricular outflow tract obstruction seen in HCM. Patients with apical HCM may present with angina, heart failure, myocardial infarction, syncope, or arrhythmias and are typically managed with medications like verapamil and beta-blockers for those who have symptoms and antiarrhythmic agents like amiodarone and procainamide for treatment of atrial fibrillation and ventricular arrhythmias. An implantable cardioverter defibrillator (ICD) is recommended for high-risk HCM patients with a history of previous cardiac arrest or sustained episodes of ventricular tachycardia, syncope, and a family history of sudden death.
There are several causes of troponin elevation other than acute coronary syndromes. Some of the common noncoronary ischemia-related causes include chronic renal failure, advanced heart failure, acute pulmonary embolism, acute inflammatory myocarditis, and coronary artery vasospasm. Apical hypertrophic cardiomyopathy (HCM) is one of the rare cardiomyopathies which can also present like an acute myocardial infarction (MI). We present a case of 66-year-old female who presented with chest pain to our emergency room and was found to have apical hypertrophic cardiomyopathy.
A 66-year-old independently functioning woman presented to the emergency room with an episode of midepigastric and left sternal chest pain. Her medical history included hypertension, hyperlipidemia, glaucoma, and multiple previous episodes of chest pain similar to her current episode that necessitated three separate coronary angiograms which showed no stenotic or occluding lesions in the coronary arteries. The patient described her chest pain as a sensation of burning that started suddenly at 11 pm in the night while she was resting comfortably at home after having dinner. The pain was mild in intensity, nonradiating, and lasted for a few minutes before resolving spontaneously. She denied having any dyspnea, palpitations, dizziness, or loss of consciousness during this episode. She had no history of smoking or illicit drug use. Her home medications included felodipine extended release 5 mg once daily, isosorbide mononitrate extended release 30 mg once daily, atorvastatin 80 mg once daily, losartan 100 mg once daily, hydrochlorothiazide 25 mg once daily, and metoprolol succinate extended release 100 mg once daily. The patient activated emergency medical services immediately after onset of her symptoms, who brought the patient to the emergency room. On arrival in the emergency room, the patient was asymptomatic. Her vital signs were as follows: blood pressure of 168/46 mmHg (right arm, supine position), heart rate of 66/min, respiratory rate of 19/min, and an oral temperature of 97.9 F. An electrocardiogram was obtained which showed a normal sinus cardiac rhythm with a left bundle branch block, possible left ventricular hypertrophy, and T wave inversions in the lateral leads. No ST segment changes were noted (Figure
Initial EKG showing normal sinus cardiac rhythm with a left bundle branch block, possible left ventricular hypertrophy, and T wave inversions in the lateral leads. No ST segment changes were noted.
Follow-up EKG showing no changes compared to the first EKG.
Coronary angiogram showing normal left main, left anterior descending, left circumflex, and right coronary arteries with no stenotic or occluding lesions.
Cardiac left ventriculogram done by cardiac chamber catheterization confirming the echocardiographic finding of apical hypertrophy.
Apical hypertrophic cardiomyopathy is a variant of hypertrophic cardiomyopathy in which the hypertrophy of the myocardium predominantly involves the apex of the left ventricle resulting in midventricular obstruction, as opposed to the left ventricular outflow tract obstruction seen in HCM [
While apical HCM is low on the list of suspected differentials for patients presenting with chest pain and elevated cardiac troponin levels on laboratory testing, the more common causes of such a presentation being STEMI or NSTEMI, this case still demonstrates the importance of following the proper testing protocol for patients who present with these findings to the emergency room—namely, an EKG, followed by testing for cardiac troponin levels, a bedside echocardiogram, and an urgent coronary angiogram if EKG changes are seen along with elevated cardiac troponin levels. For patients with no EKG changes and elevation in cardiac troponin levels, they should still be treated as an NSTEMI with anticoagulation and an early coronary angiogram preferably within 24 hours of presentation, especially if they have clinical findings that are strongly suggestive of an NSTEMI, i.e., symptoms of ischemic chest pain on presentation and prior risk factors of coronary artery disease.
The approach to the management of apical HCM is the same as for most patients with HCM; symptomatic patients are initially treated with medical therapy, which includes medications like verapamil and beta-blockers [
Apical HCM is a variant of HCM in which the hypertrophy of the myocardium predominantly involves the apex of the left ventricle resulting in midventricular obstruction, as opposed to the left ventricular outflow tract obstruction seen in HCM. While apical HCM has a better mortality prognosis than other forms of HCM, it is still associated with a relatively high rate of important cardiac events like atrial fibrillation or myocardial infarction. Apical HCM is low on the list of suspected differentials for patients presenting with chest pain and elevated cardiac troponin levels on laboratory testing, the more common causes of such a presentation being STEMI or NSTEMI. This case demonstrates the importance of following the proper testing protocol for patients who present with these findings to the emergency room—namely, an EKG, followed by testing for cardiac troponin levels, a bedside echocardiogram, and an urgent coronary angiogram if EKG changes are seen along with elevated cardiac troponin levels. The approach to the management of apical HCM is similar to most patients with HCM—medical therapy for symptomatic patients, which includes medications like verapamil and beta-blockers and antiarrhythmic agents such as amiodarone and procainamide for treatment of atrial fibrillation and ventricular arrhythmias. Since apical HCM does not involve LVOT obstruction, septal reduction therapy is almost never used to treat apical HCM. The risk of ventricular tachyarrhythmias and sudden cardiac death is low in apical HCM, and an implantable cardioverter defibrillator (ICD) is only recommended for high-risk HCM patients with a history of previous cardiac arrest or sustained episodes of ventricular tachycardia, syncope, a family history of sudden death, or episodes of nonsustained ventricular tachycardia on serial Holter monitoring.
The authors declare that they have no conflicts of interest.