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Sumario Vol. 42 - Nº 2 Abril - Junio 2013

Coronary Spasm Induced by Dobutamine
Stress Echocardiography

Javier Courtis, José Tibaldi, Alejandro Sarría Allende

Instituto Oulton (Córdoba) - Clínica Romagosa (Córdoba).
Instituto Oulton: Av. Vélez Sarsfield 562 (5000)
Córdoba Capital, Argentina.
Tel: 351-4267700 (int 183). Fax: 351-4267765
Correo electrónico

The authors declare not having a conflict of interest.
 


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SUMMARY

Dobutamine stress echocardiography (DSE) is a useful tool in evaluating patients with possible coronary artery disease, ST segment elevation during this test is a rare complication and almost always associated with severe coronary artery disease. However, if there is no angiographic evidence of severe coronary obstruction, it is believed that this complication would result from coronary spasm. We present the case of a 52-year-old man who presented, during a DSE, severe chest pain with ST segment elevation, impaired left ventricular contractility and coronary angiography without severe obstructive coronary disease.

Key words: Dobutamine.Stress echocardiography.Coronary spasm.
Rev Fed Arg Cardiol. 2013; 42(2): 150-154

 

 

INTRODUCTION
Stress echocardiography with dobutamine (DSE) is a useful tool in the evaluation of the patients with probable CAD due to its high sensibility to detect myocardial ischemia and its excellent security profile. Dobutamine is a well tolerated catecholamine, with a very short half life (2-3 min) and a very low rate of severe complications during DSE. In the case of adverse effects presenting, they are usually related to ischemia or arrhythmias induced by the drug [1] The evaluation of myocardial ischemia induced by pharmacological stress is generally based on the detection of new alterations in ventricular segmental motility observed in 2-dimensional echo. These contractile and transient dysfunctions are the result of an imbalance between the offer and the demand of oxygen, during the infusion of the drug, and are frequently associated to ST segment depression in the ECG. On the contrary, ST segment elevation during DSE is very infrequent and nearly always is associated to severe ischemic heart disease (IHD). In absence of atheromatous coronary obstruction, a very infrequent finding, ST segment elevation would be due to a marked spasm in a coronary artery [2-4]. We present the case of a 52-year-old man, who presented severe chest pain during DSE with significant ST segment elevation in ECG inferior leads and evident segmental disorders in the inferior side of the left ventricle (LV) in the echocardiographic recording. In spite of these changes, cine coronary angiography of emergency did not show severe IHD, except for a muscular bridge on the Anterior Descending artery (ADA), a territory not involved according to the ECG analysis.


CLINICAL CASE
A 52-year-old man, former smoker, with history of hypertension and mild mixed dyslipidemia, was referred for a DSE to evaluate atypical chest pain without anomalies in ECG made 20 days before the procedure. The patient did not mention having chest pain over the last 48 h prior to the stress test. In rest, before the test, the patient presented blood pressure (BP) of 125/75 mmHg and the basal ECG only showed sinus bradycardia with the rest of the tracing without other particular aspects (Figure 1A). The initial images of echocardiography (Figure 2A) showed cardiac chambers of a normal size, preserved systolic function, and absence of anomalies in segmental contractility. DSE was made according to the institutional protocol. The infusion of IV dobutamine started at 5 µg/kg/min and was gradually increased to 10, 20 and 30 µg/kg/min every three minutes. At the time of the 30 µg/kg/min of dobutamine, the patient presented sudden and very intense chest pain, accompanied by neurovegetative signs (profuse sweating and nausea). At the time, the heart rate was 159 bpm (91% of maximal heart rate, estimated as 220 – age in years), the blood pressure of 130/85 mmHg and the ST segment of ECG showed a >2 mm elevation in the DII, DIII, aVF, V5 and V6 leads, and a >1 mm depression in DI, aVL and from V1 through V4 (Figure 1B). The echocardiogram showed severe hypokinesis of all the inferior wall and the inferoseptal medial segment (Figure 2B). The infusion of dobutamine was immediately interrupted, 5 mg of sublingual isosorbide dinitrate and IV infusion of nitroglycerin was started. After administering this medication, chest pain started to yield gradually, but ST segment elevation persisted for ten minutes and ventricular segmental motility alterations remained for another twenty minutes. Since the symptoms continued, the patient was immediately sent to the hemodynamic room where oral aspirin 500 mg, clopidogrel 600 mg and sodium heparin 5000 UI were administered. Cine coronary angiography (CCA) using right transradial access pathway (5F) and appropriate diagnostic catheters (JL, JR and pigtail). Angiography showed a mild lesion (20-40%) in the middle third of theADA immediately before an extensive systolic contraction (25 mm of longitude) of this coronary artery that normalized during the diastole (myocardial bridge). The Circumflex artery did not present angiographically evident lesions, and the Right Coronary artery (dominant) only showed parietal irregularities in its distal segment with no severe obstruction throughout its extension (Figure 3). The provocation test with methylergometrine was not made.

Subsequently, the patient remained hospitalized for 12 hours in the coronary unit, where he was treated with oral ASA 100 mg/day, atenolol 25 mg every 12 hours, rosuvastatin 10 mg/day. The total creatine phosphokinase (CPK) and myocardial band (CPK-MB) enzymes remained in normal values 12 h after the pain started. The patient had a satisfactory clinical evolution and was discharged 36 hours after the symptoms started. Two days after the DSE, an echo showed preserved global and segmental contractility with normal left ventricular function. In the subsequent controls during the follow-up, the patient did not mention having precordial pain.

Figure 1. Twelve-lead ECG
1a. Corresponds to basal ECG and only sinus bradycardia stands out in a normal tracing
1b. During the infusion of 30 µg/kg/min of dobutamine, it shows ST segment elevation greater than 2 mm in the DII, DIII, aVF, V5 and V6 leads and depression greater than 1 mm in DI, aVL and from V1 through V4.

 

Figure 2. Stress echo with dobutamine
2a. In column A, the left ventricle is seen in basal conditions in different views without contractility alterations.
2b. In column B, severe hypokinesis of all the inferior side is seen during the 30 µg/kg/min infusion of dobutamine.

 

Figura 3. Cine coronary angiography by right transradial pathway. Figures A and B correspond to the left coronary arteries. A mild lesion is seen in the middle third of the Anterior Descending artery immediately before an extensive myocardial bridge (white arrow) and the Circumflex artery without angiographically evident lesions. The Right Coronary artery, dominant, does not present severe obstructions throughout its extension (figure C).

 

DISCUSSION
The clinical case described is the example of a patient with incipient coronary atherosclerosis that presented coronary spasm induced by adrenergic stimulation during DSE as a consequence of endothelial dysfunction. Although the patient presented a muscular bridge in the ADA, both electrocardiographic alterations and ventricular segmental motility disorders may be explained by a vasoconstriction phenomenon at the level of the Right Coronary artery and not by exaggeration of the systolic compression of the muscular bridge. A limitation in the analysis of this case was that the intracoronary methylergometrine test was not made during CCA before the suspicion of spasm.

DSE is a highly accurate test made for the diagnosis of CAD, with a sensibility of 88% and a specificity of 83% [5,6]. Its indications have remarkably increased over recent years, giving rise to more stress tests and therefore, a greater number of complications. Several secondary effects may happen during DSE, among the most common are hypertension and arrhythmias; and among the least frequent are myocardial infarction, hypotension and coronary arteries spasm [7]. ST segment elevation settling in this stress test has been documented in 30-55% of patients with prior myocardial infarction and pathological Q wave in ECG [8,9]. In patients without prior myocardial infarction, ST segment elevation during DSE is an infrequent finding, in up to 6% of the cases [10], which is usually associated to atheromatous and critical obstruction of a coronary artery [11]. In absence of obstructive and severe CAD, ST segment elevation is even rarer, and to the present only some cases have been reported in literature [12-14].

In a recent study, Mansencal et al [15] evaluated the prevalence of coronary spasm in 2,179 individuals referred for DSE and they systematically analyzed all the electrocardiograms obtained during the test. Just 1% of the patients (n=21) presented ST segment elevation and all them underwent emergency cine coronary angiography. In 13 of these 21 patients (62%), significant coronary stenosis (6 cases with critical stenosis and 7 with chronic coronary occlusion) was observed. The 8 remaining patients (38%) had no significant coronary stenosis, with ST segment elevation being interpreted as a result of coronary spasm. The authors concluded that the prevalence of coronary vasospasm during DSE was 0.4%, which confirms that this vascular functional alteration is very infrequent during this test.

Usually, the sudden presence of chest angina, ST segment elevation and ventricular parietal motility anomalies during DSE correspond to coronary vasospasm.

In those patients with severe CAD, the previously described anomalies generally occur gradually and may even occur with the use of low doses of dobutamine and worsen as the myocardial oxygen consumption increases. The interruption of the test and the use of appropriate medications helps to prevent myocardial infarction.

The pharmacodynamic action of dobutamine in the coronary arteries is mainly vasodilator by stimulation of β1-adrenergic receptors in the presence of vascular endothelium functioning normally; however, on certain occasions it may induce paradoxical arterial spasm. An explanation for this phenomenon could be that in the presence of endothelial dysfunction there is a change in vasomotor function and an increase in α1 stimulus, which would lead to the loss of the vasodilator effect of the drug in favor of a vasoconstrictor response [16]. Gordon et al [17], showed that the segments of the coronary arteries with parietal irregularities respond to exercise and to acetylcholine with spasm, which expresses local endothelium dysfunction. Another explanation is that at high doses, dobutamine may cause anxiety in up to 6% of the patients [18], which may lead to hyperventilation and thus generate respiratory alkalosis that causes an increase in the exchange of Na+/Ca2+, leading to an increase in the concentration of intracellular Ca2+ that results in the vascular smooth muscle contracting [19]. Although dobutamine may unmask vasospastic chest angina, curiously coronary spasm may also be considered an adverse effect of the drug. So much so that in the report by Mansencal et al [15], only 3 from 8 patients with coronary spasm induced by DSE were asymptomatic before the test and DSE was carried out to evaluate the pre-operative risk. In these individuals, the induced spasm was clearly a secondary effect of the test. On the contrary, the other 5 patients with ST segment elevation and without angiographic stenosis of coronary arteries presented chest pain before the DSE, being interpreted that in these patients dobutamine unmasked vasospastic angina, which allowed its diagnosis. For this reason, the authors consider that saving the datum of precordial pain prior to the stress test would allow differentiating between vasospastic angina and adverse reaction to dobutamine in those patients that develop precordial pain with ST segment elevation and coronary arteries without severe obstructions in angiography.

Finally, the long-term prognosis of the patients with ST segment elevation, during DSE, depends on whether the clinical symptoms are a consequence or not of atherosclerotic ischemic heart disease with severe involvement of the coronary artery tree. In the case of being secondary to coronary spasm, the prognosis is good [4]; not so if the electrical and contractile alterations are the expression of severe ischemic heart disease [8], in which case, the patients present an increased risk of presenting cardiovascular events in the long term.


CONCLUSIONS
In spite of its high security profile, DSE may on certain conditions, induce coronary artery spasm generating as a consequence, precordial pain with significant electro and echocardiographic alterations.

Coronary spasm caused by dobutamine, an infrequent situation, is the result of alpha-adrenergic stimulation on a dysfunctional endothelium, with a good prognosis in the short term.

Nitrates by the intravenous pathway, are probably the cornerstone of the initial treatment. The provocation test with methylergometrine is a safe and efficient technique that allows establishing a definitive diagnosis.

 

 

REFERENCES

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Publication: June 2013

 
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