CASE REPORT

Angina pectoris in patient with hyperthyroidism and angiographically normal coronary arteries

Alessandra Ferri Casini; Ilan Gottieb; Leonardo V. Neto; Carla A. Almeida; Regina H. A. Fonseca; Mario Vaisman

Hospital Universitário Clementino Fraga Filho – UFRJ, Rio de Janeiro, RJ, Brazil

Mailing Address

ABSTRACT

The presence of angina pectoris in a premenopausal woman with no other major risk factors for coronary heart disease demands that we rule out other causes for non-atherosclerotic coronary lesions. The relationship between hyperthyroidism and cardiovascular abnormalities is well established, but hyperthyroidism accounts for less than 5% of cases of chest pain. This study is about a female patient, 47 years of age, with typical symptoms of precordialgia and an electrocardiogram (EKG) suggestive of coronary ischemia, but whose laboratory tests showed no abnormalities that might indicate myocardial injuries. The anamnesis, physical examination and laboratory results helped to confirm the diagnosis of hyperthyroidism. Subsequent cardiac catheterism did not show any obstructive lesions. After treatment with radioactive iodine (radioiodine) and a return to euthyroidism, the patient remained asymptomatic, and both the EKG and myocardial scintigraphy were negative for ischemia. These results propose an interaction between thyroid hyperactivity and myocardial ischemia, implying that hyperthyroidism might be the probable etiology for the clinical and electrocardiographic findings.

Key words: Hyperthyroidism, angina pectoris, electrocardiogram, coronary arteries.

The relationship between ischemic cardiopathy and hyperthyroidism has already been described, although not totally explained. In spite of hyperthyroidism accounting for less than 5% of all cases of cardiac origin chest pain¹, the fact that the thyroid hormone can directly affect the factors that determine the consumption of oxygen by the myocardium, even when there is no apparent cardiac disease, may result in angina pectoris and, less commonly, acute myocardial infarction.

The prevalence of hyperthyroidism in the general populationvaries from 0.5% to 1%². We report a case of coronarysyndrome due to vasospasm in a female patient withhyperthyroidism that did not have any other risk factors forcoronary disease.

Case Report

An 47-year-old female presented with clinical symptoms ofnervousness and palpitation associated with excess sudoresis andinsomnia for approximately one year. She also reportedoligomenorrhea, but no gonadal function abnormalities wereobserved upon gynecological evaluation (FSH = 2.34 mIU/ml and LH= 3.64 (mIU/ml). The patient was subsequently referred to anendocrinologist. She had been previously hospitalized six timesdue to resting retrosternal pain with three minutes of duration,not associated with vagal symptoms, and responsive to treatmentwith nitroglycerin. She denied the use of medications, even oralcontraceptives, up until the beginning of the angina symptoms,when she started using 10 mg of isosorbide dinitrate twice a day,acetylsalicylic acid 200 mg/day, atenolol 50 mg/day, andcaptopril 12.5 mg/day. She had a positive family history forthyroid disease, although there were no cases of cardiopathy ordislipidemia. She reported being an occasional smoker (one or twocigarettes a day).

The physical examination from the previous hospitalizationrevealed a regular triphasic cardiac rhythm, presence of a fourthheart sound, arterial blood pressure 120/70 mmHg, heart rate – 98bpm, fine tremors of the extremities, and characteristically hotthin skin. The volume of the thyroid gland was augmented due to anon painful mobile nodule measuring approximately two centimetersand located at the upper pole of the right lobe. The remaininggland had a smooth surface and elastic consistency. Absence ofcervical adenomegaly.

During the angina episodes, including those in previous hospital admissions, the electrocardiogram (EKG) showed T-wave inversion from V1 through V4, and ST-segment elevation from V2 through V3 (figure 1). Laboratory results did not suggest myocardial lesions. CK 41 U/l, 92 U/l (21-215 U/l), CKMB 0 U/l, 2 U/l (0-20 U/l), troponine 0 ng/ml (0.1-0.5 ng/ml), TGO 19 U/l, 15 U/l (15-37 U/l). The patient was diagnosed with acute coronary syndrome and therapy was initiated with antiaggregant agents, heparinization, intravenous nitroglycerin and beta-blockers. She responded well to therapy in all episodes of pain. During her last hospitalization, the echocardiogram showed mid-apical septal hypokinesia, mild aortic insufficiency and minimal mitral insufficiency. The coronariography and ventriculography showed that the left ventricular systolic function was preserved and the coronary arteries were free of obstructive lesions.

The echocardiogram performed eight days after the first onewas completely normal, and the EKG normalized a few times duringthe periods without pain. Lipid profile: TC 178 mg/dl, LDL 113mg/dl, HDL 49 mg/dl, TG 82 mg/dl. Hyperthyroidism was confirmedby laboratory tests: T4L 2.57 ng/dl (0.8-1.9 ng/dl), TSH 0.099uU/ml (0.40-4.00 uU /ml). Thyroid scintigraphy showed 24-hour¹³¹ I uptake of 21.26% and an accumulation ofradioactive material almost entirely in the right lobe,suggesting toxic nodular goiter. The patient was submitted to atherapeutical dose of ¹³¹ I 18.8 mCi and asupplemental treatment with propylthiouracil (initial dose of 400mg/day) during the following five months, after which the patientbecame euthyroid again.

The EKG (Fig. 1) and perfusion scintigraphy with ^99mTc at rest, and after pharmacological stress with dipyridamole, performed immediately after the return to euthyroidism (T4L 1.39 ng/dl, TSH 2.24 uU/ml) were negative for myocardial ischemia. Since then, the patient has been clinically asymptomatic.

Discussion

The cardiovascular system and thyroid hormone are closelyrelated. Mild alterations in the thyroid function markedly affectthe contractility and electrical activity of the heart.

The cardiovascular hemodynamic effects from the excess thyroidhormone result mainly from the direct action of T3 oncardiomyocytes by binding to its receptor, especially thealpha-1-TR isoform (genomic action), and indirect action throughsympathetic effects such as an increase in sensitivity tocatecholamines, increase of the number of beta-adrenergicreceptors, and decrease of the alpha-adrenergic receptors in themyocardium; formation of free radicals and oxygen consumptionresulting in an increased basal metabolism rate due tostimulation of NA/K/ATPase, besides the effects on vasculaturesuch as reduction of the peripheral vascular resistance andaccelerated venous return³.

There are several cardiovascular manifestations ofhyperthyroidism: sinus tachycardia (invariably the most frequentfinding), systolic arterial hypertension, abnormalities in thesystolic and diastolic ventricular function, arrhythmias (mainlyatrial fibrillation), and coronary insufficiency. In the greatmajority of cases, such abnormalities recede after the control ofhyperthyroidism.

In the context of hyperthyroidism, coronary insufficiency isrepresented by angina pectoris and acute myocardial infarction.Although angina affects approximately 0.5% to 20% of thepatients, myocardium infarction is extremely uncommon, with onlya few cases reported in medical literature (an incidence ofapproximately 1.8 %)⁴. Descriptions of case reports,typically affecting women under 40 years of age, depict coronaryarteries free of lesions on the coronariography^5-7,such was the case of our patient.

However, the physiopathology mechanisms have not yet been totally explained. There is evidence that the thyroid hormone may affect the factors that determine the consumption of oxygen by the myocardium³, and that abnormalities in oxygen-hemoglobin dissociation could explain such a fact. Other possible mechanisms are: ischemia secondary to coronary vasospasm^5,6,8 due to an unbalance in the autonomic cardiac innervation, a modification in the concentrations of tromboxane A, and prostacycline in the coronary circulation, with insufficient vasodilation to supply the metabolic demand⁹, microvascular disease and thromboembolism with posterior recanalization of the arterial lumen. Although uncommon, there are other non-atherosclerotic causes for the obstruction of the coronary arteries such as vasculitis, rheumatic diseases, syphilis, use of cocaine, Prinzmetal angina, which would be considered as differential diagnoses in the case described. Moreover, if the patient did not have a palpable node on physical examination or a family history of thyropathy, some of the reported symptoms could lead to the hypothesis of climacterium. However, the remission of angina after the hyperthyroidism treatment associated with the patient's normal coronaries and ruling out all other etiologies, suggest coronary vasospasm resulting in myocardial angina. Therefore, all this considered, we feel it should be mandatory to rule out any thyroid pathology, particularly in premenopausal women with symptoms of cardiopathy in the absence of other coronary risk factors.

References

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Mailing Address:
Alessandra Ferri Casini
Av. Doutor Pedro Feu Rosa, 501/ 102
29060-730 – Vitória, ES, Brazil
E-mail: ale.casini@ig.com.br

Manuscript received July 1, 2005; revised Manuscript received March 3, 2006; accepted March 7, 2006.