Unexpected Grave’s-induced acute myocardial infarction in a young female, a literature review based on a case report

Abstract

Introduction

Myocardial ischemia can occur due to several causes, which result in an imbalance between the supply and demand of oxygen to cardiac muscles. One potential reason for this condition is the overwork of the heart due to hyperstimulated thyroid function.

Case presentation

The patient was a 36-year-old woman who presented with left-sided chest pain, dyspnea, palpitation, and tremor. The initial evaluation showed evidence of myocardial ischemia (positive high-sensitivity troponin) caused by a hyperactive thyroid gland. The treatment for myocardial infarction, along with anti-thyroid medications, improved the patient’s condition and subsided the symptoms. The coronary angiography revealed no pathologic finding, and the hypokinetic left ventricle, observed in the first echocardiogram, was resolved. The patient was discharged with an excellent clinical condition, and after the 4-month taking of a calcium channel blocker and tapering carbimazole, the thyroid function became normal, and her symptoms resolved completely.

Conclusion

Patients without evident risk factors for ischemic heart disease, such as non-diabetic, nonsmoker, and young individuals who presented with acute coronary syndrome, should be evaluated for a potential background reason for the imbalance between the oxygen demand and supply of the myocardium. The presence of palpitation, weight loss, tremors, insomnia, and anxiousness, along with ischemic signs, should make the physician think about the probability of the hyperthyroid-induced cardiovascular disorder.

Clinical key point

The initial presentation of hyperthyroidism might be accompanied by severe cardiac symptoms. When the demographic features are not aligned with usual ischemic heart disease, other probable symptoms and signs should be investigated, and thyroid function should be checked. The control of thyroid hyperactivity would result in the resolution of both cardiac and non-cardiac symptoms.

Introduction

Type II myocardial infarction (MI) is defined by the activation of imbalance triggered by secondary causes, including accelerated metabolism and demand for more blood circulation due to sepsis, drugs, hypoxemia, and hyperthyroidism [1]. The increased demand for oxygen is caused by increased metabolism in myocardial tissue, which works faster and stronger in response to the overstimulation of thyroid gland products. This effect is caused by the enhancement of mitochondrial production, increased activity of intrinsic enzymes, and the development of intracellular proteins [2]. These all can lead to imbalanced myocardial bioenergetic condition and the consequent ischemia [3]. Moreover, overwork of the thyroid gland can cause coronary vasospasm, which is a predisposing factor for coronary thrombosis secondary to and stasis of blood [4]. Another potential declared etiologies is the probability of thrombotic status activation by thyroid hormones [4]. This type of cardiovascular disease is also categorized as myocardial infarction due to non-obstructive coronary artery (MINOCA) [5].

It has been shown that the risk of cardiovascular diseases, including MI, has been considerably higher in patients with hyperthyroidism, regardless of their gender and age [6]. Interestingly, the initial presentation in 6% of patients with hyperthyroidism was myocarditis and even more than with other cardiovascular presentations such as arrhythmia, congestive heart failure (CHF), and dilated cardiomyopathy [7]. These patients prevalently experience noncardiac symptoms, including weight loss, insomnia, anxiousness, and tremors [8]. The severity of symptoms and the effect on the myocardial tissue varies between patients, ranging from intermittent chest pains without any significant injury to the cardiac muscle to a severely destroyed myocardium by ischemic attack [9, 10]. It is crucial to differentiate the cause of these ischemic attacks from the usual obstructive ones, considering the completely different management they require [11].

In this study, we present a case of undiagnosed and mismanaged thyrotoxicosis-induced myocardial infarction, presented with chest pain, palpitation, and dyspnea.

Case presentation

A 36-year-old woman with no prior medical illness presented to the Emergency Department (ED) with a sudden onset of severe left-sided chest pain that started 30 min before her arrival at the ED, present at rest and worsened by exertion, associated with palpitations, diaphoresis, and dyspnea. Over the preceding three months, she had palpitations and tremors and lost 4 kg of weight. However, the condition was misdiagnosed as general anxiety disorder, and he was referred for psychological treatment, which was ineffective. She denied the use of illicit drugs. She had never been a smoker and worked in an office with minimal physical activity. There was no remarkable point in her family history except for diabetes mellitus (DM II) in her mother. She had a history of bariatric surgery due to obesity. On general appearance, she was anxious, diaphoretic, and shaking in the upper and lower extremities. In the vital signs evaluation, a blood pressure of 158/96 mmHg, respiratory rate of 25 per minute, heart rate of 122 beats per minute, and temperature of 36.8. Cardiovascular and respiratory system examinations were otherwise unremarkable. She had exophthalmos and a diffuse goiter measuring 9 × 6 cm, without any bruit. No other remarkable finding was detected during the patient’s physical exam.

Immediately after the initial presentation and with the provisional diagnosis of Hyperthyroidism-Induced acute coronary syndrome, an electrocardiogram (ECG) was obtained, which showed sinus tachycardia without any significant ST-segment change in any of the precordial and limb leads (Fig. 1) The patient was monitored with cardiopulmonary monitoring. Lab data were requested after taking the blood sample. The patient was given oxygen via nasal canola 4-6lit/min, Metoprolol (50 mg), Aspirin (325 mg), Clopidogrel (300 mg), Atorvastatin (80 mg) orally, and Nitroglycerin (intravenous, 5 μg/min), losartan (25 mg twice a day), and UFH (5000IU stat, and 1000IU/hour). The patient’s condition improved significantly after these interventions. The patient’s blood results came back, demonstrating positive high-sensitivity cardiac Troponin I (hs-cTnI) with 98.5 (pg/ml), very high T3, T4, and considerably below the range of TSH (Table 1) A transthoracic echocardiogram (TTE) showed a hypokinetic anteroseptal wall with an ejection fraction of 35%, no valvular pathology, normal chamber sizes, and no remarkable abnormality in ventricular dimensions without any evidence of left ventricular hypertrophy (Table 2). She was treated for non-ST elevation myocardial infarction and hyperthyroidism. The serial ECG was done every 30 min, and it showed non-specific ST-segment changes in limb and precordial leads, which were detectable on the 4th ECG (Fig. 2) The changes were suggestive of probable ischemic changes in the myocardium.

The neck (thyroid and lymph nodes) ultrasound imaging showed a diffusely enlarged thyroid, increased vascularity, and diffused hyperactivity (Table 3) The coronary angiography (CA) 48 h after the patient’s presentation revealed no abnormal findings (Fig. 3).

Fig. 1

The initial electrocardiogram showed sinus tachycardia without any other remarkable finding

Fig. 2

The 4th electrocardiogram, performed 90 min after the initial electrocardiogram, showed dynamic changes in limbs (blue arrows) and precordial (red arrows) leads

Fig. 3

The coronary angiography of the patient showed no abnormal finding

Table 1 Index laboratory data

Table 2 The patient’s echocardiogram showed evidence of hypokinetic myocardium

Table 3 Thyroid ultrasound showed the diffuse hyperactivity without any nodule

Due to the unavailability of the anti-TSH receptor antibody in the hospital’s laboratory, it could not be checked. However, these antibodies were evaluated, and the thyroid radionuclide scan was performed after discharge, which was compatible with the diagnosis of Grave’s disease. The laboratory workup showed that the patient had decreased thyroglobulin (Tg), 0.10 μg/L, with positive thyroglobulin antibody (Tg-Ab), positive thyroid peroxidase antibody (TPO-Ab), and positive thyroid-stimulating hormone (TSH) receptor antibody (TR-Ab). The thyroid radionuclide scan was performed, which showed disseminated hyperactivity of the thyroid, which was compatible with the diagnosis of Grave’s disease. The tablet carbimazole 30 mg daily, which was started after stabilizing the patient’s condition in the hospital, was gradually tapered over six months, and verapamil 80 mg was continued despite the discontinuation of all other medications. Considering the differential diagnosis of myocarditis, an echocardiogram and cardiac magnetic resonance imaging (CMRI) were performed, which showed no sign of myocarditis. During the follow-up sessions 2, 4, and 8 weeks later, she had no new complaints and remarked on good activity tolerance. The thyroid function was normal at the 4th follow-up visit four months after the admission. Repeat ECG (Fig. 4) and TTE showed no remarkable abnormality. Normal chambers, valvular function, and an ejection fraction of 50% were detected on the TTE. The detected hypokinetic area in the initial ER echocardiogram was not observed in the follow-up TTE.

Fig. 4

Resolution of tachycardia and ST-segment changes in the follow-up ECGs

Discussion

In this case report, we presented a patient with undiagnosed graves, presented with cardiovascular symptoms and NSTEMI. Although the prevalence of thyrotoxicosis-induced MI is less than 2%, it has substantial importance considering the cruciality of differentiation from obstructive ischemia [9, 10]. The broader term for such cardiovascular disorders is MINOCA, defined by 1) myocardial infarction approved by documents, 2) approval of the absence of obstructive coronary arteries, and 3) the exclusion of any other background cause e for the AMI presentation, such as cardiac trauma [12]. However, the symptoms and clinical manifestations might be less severe, causing recurrent angina, known as thyrotoxicosis angina. The diagnostic criteria include four conditions: (I) lack of clinical presentations of hyperthyroidism at presentation, (II) rapid and progressive angina, iii) presence of pain at rest, and IV) resolution of symptoms after treating hyperthyroidism [13].

The most common background cause of thyrotoxicosis is Grave’s disease, which is related to myocardial ischemia [14]. The underlying pathophysiology of this condition is the abnormal production of thyroid-stimulating Antibody (TSAb), also known as thyroid-stimulating immunoglobulin (TSI). The attachment of the immunoglobulin to the TSH receptors results in both the enlargement and increased secretion of the thyroid hormones, causing thyromegaly and hyperthyroidism [15]. The diagnosis of this condition relies on the history and physical examination along with laboratory data and imaging. Suppressed TSH, highly elevated T3, T4, and positive TSAb are diagnostic methods laboratory indicators [15].

The vasospasm caused by thyrotoxicosis might be intermittent and not be seen during the CAG. However, it is the main method of diagnosis. The absence of occlusion and probable vasospasm, which are reactive to the intracoronary infusion of nitroglycerine, are other associated diagnostic hints of Grave’s-induced vasospasm and myocardial ischemia. In case of inconclusive CAG results, intravascular ultrasound (IVUS) or optical coherence tomography (OCT) can be beneficial for the differentiation of the obstructive and non-obstructive causes of MI [14]. Stress-induced cardiomyopathy is another differential diagnosis that should be ruled out in these cases (Takotsubo). It can be achieved by imaging strategies such as TTE, Cardiac magnetic resonance imaging (CMRI), and CAG [16].

The main recommended medications for treating these conditions are combined antithyroid medications (Methimazole, Carbimazole), Calcium channel or beta blockers, corticosteroids, and symptomatic therapy. Although treatment with beta-blockers is a standard part of Hyperthyroidism-Induced tachycardia, it is controversial, considering the evidence of worsening symptoms in some cases. Aspirin and nitroglycerin long-time use, considering the uncertainty of their effectiveness, is not recommended, although there is no common consensus regarding their impact on these conditions [17]. A study conducted by Al Jaber et al. showed that these patients have an excellent prognosis with the application of appropriate anti-thyroid treatment [18]. Table 4 provides more information regarding the similar cases.

Table 4 Hyperthyroidism-Induced Acute Coronary Syndrome Literature Review

Clinical key point (conclusion)

Grave’s disease, along with other types of hyperthyroidism, can result in ACS and, in severe cases, myocardial ischemia and infarction. The presentation might be without or with subtle extracardiac symptoms such as weight loss, tremors, insomnia, and anxiousness. It is recommended that patients with ACS symptoms be screened for secondary MI. Considering their different treatment, these MINOCA cases should be diagnosed and differentiated from the occlusive instances of myocardial infarction.