Case Report

Severe chest pain during stress dobutamine echocardiogram in patient with patent epicardial coronary arteries

Abstract

Dobutamine induced ST-segment elevation in the absence of obstructive coronary artery disease is a Rare condition. We report a case of a 37-year-old man, a smoker, who developed severe chest pain associated with transient ST-segment elevation in anterolateral leads and significant segmental wall motion abnormalities during dobutamine stress echocardiography that was immediately relieved by sublingual nitrates without evidence of acute myocardial infarction. coronary angiogram showed patent epicardial coronary arteries.

Dobutamine-atropine stress echocardiography (DBS) is a well-known tool for the assessment of patients with a questionable coronary artery disease. Dobutamine is a well-tolerated catecholamine, with very short half-life of 2 to 3 minutes. The rate of serious complications during DBS is low and similar to that described with conven- tional stress tests. The complications that usually present during the performance of DBS tend to be related to ischemia or arrythmias induced by dobutamine [1-3]. The evaluation of stress-induced myocardial ischemia is based on the detection of decreased myocardial systolic thickening by 2-dimensional echocardiography. These wall motion abnormalities are induced by an unbalance between oxygen Supply and demand during stress. The presence of ST-segment deviation in 12-lead electrocar- diogram (ECG), in association with transitory wall motion

Fig. 1 Electrocardiographic changes during DBS: A, Baseline ECG. B, ST elevation during DBS at 1, aVL, and V₄ through V₆. C, ST elevation; 1, aVL, and V₂ through V₆ with severe chest pain. D, Electrocardiogram at recovery; resolution of ST elevation 2 minutes after sublingual nitrate.

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abnormalities, is an uncommon finding during DBS and generally indicates severe coronary obstruction. However, it is already known that the increase in arterial shear stress during DBS may lead to Coronary spasm even in patients with no significant coronary obstruction [1-3]. However, during DBS, momentary alterations of myocardial wall motion can occur in the absence of electrocardiographic changes; or they may be associated with ST-segment changes on the ECG. Herein, we describe a young male patient who sustained severe chest pain and ST-segment elevation during DBS.

A 36-year-old male patient is known to have a history of hypertension and cigarette smoking for more than 10 years. The patient reported one episode of chest pain 6 months before last admission. At that time, the result of his ECG was normal with negative cardiac markers. Treadmill test was inadequate and terminated prematurely because of exercise intolerance. Coronary angiogram revealed patent epicardial coronary arteries. Because of recurrence of chest discomfort, the patient was referred for DBS. The patient was free of chest pain in the few days

preceding the stress test. Resting heart rate was 80 beats per minute, and blood pressure was 116/78 mm Hg. The result of the baseline 12-lead ECG was normal; and the echocardiogram at rest showed left ventricular hypertro- phy, normal global systolic function ejection fraction 60%, and no abnormalities in segmental wall motion. The DBS was carried out based on the following protocol. Intravenous dobutamine infusion was started at a dose of 5 ug/(kg min) and increased to 10, 20, 30, and 35 ug/ (kg min) every 3 minutes. Atropine was started at 35 ug/ (kg min) plus handgrip, at which the patient achieved target heart rate of 85% (160/min.). At 35 ug/(kg min) of dobutamine and 0.5-mg total atropine dose, the patient experienced sudden, severe Retrosternal chest pain associ- ated with nausea, vomiting, sweating, heart rate of 160/min, and maximum blood pressure of 170/70 mm Hg. The ECG showed sinus tachycardia, STE up to

4.0 mm in leads 1, aVL, and V₂ through V₅. There were reciprocal changes in ST-segment depression up to 2.0 mm in leads III and AVF. All the ECG changes normalized within 2 minutes (Fig. 1).

Fig. 2 Echocardiography images during DBS. A, Baseline. B, At load dose dobutamine. C, At peak stress. D, During recovery. Arrows indicate dyskinetic anterior septum.

Fig. 3 Coronary angiography that revealed patent left (A) and right (B) coronary arteries with nondominant right coronary artery.

At rest, echocardiogram showed normokinesia of all cardiac segments. At low dose, there was hyperkinesia of all cardiac segments except hypokinesia of midposterior septum. At peak dose, dyskinesia appeared in the anterior septum and apex. At recovery, the segmental wall motion abnormalities normalized except for hypokinesia of the

Table 1 Dobutamine-induced STE in patients with or without obstructive coronary lesions

M indicates male; F, female; RCA, right coronary artery; LAD, left descending artery; MI, myocardial infarction; LCX, left circumflex; CAD, coronary artery disease; VF, ventricular fibrillation; VT, ventricular tachycardia.

^a Atropine used.

septum that lasted for 15 minutes; after that, only apical septum showed mild hypokinesia (Fig. 2). Dobutamine infusion was interrupted, and 5 mg of nitrate was given sublingually; then chest pain dramatically disappeared, but the ST-segment shifts remained for further 2 minutes. Left ventricular wall motion abnormalities lagged for another

Author(s)	Age (n)		Sex	Risk factor(s)	Protocol stage	Territory affected	Obstructive CAD	Periprocedural event
Shaheen et al [6]	48	(1)	M	Dyslipidemia,	High a	RCA	Yes	-
				smoking
Deligonul et al [7]	35	(1)	M	Dyslipidemia,	High	RCA	Yes	VF
				smoking
Roffi et al [4]	58	(1)	M	Dyslipidemia,	Low/high	LAD/RCA	Yes	-
				smoking
Kardaras et al [8]	70	(1)	M	None	Low	RCA	Yes	-
Weidmann et al [9]	42	(1)	F	Dyslipidemia,	Recovery	RCA/LAD	Yes	Inferior MI
				smoking
Kawano et al [5]	59	(7)	5 M/2 F	-	High	LCX, RCA, LAD	No	-

Amar et al [10]	49 (1)	F	Hypertension	High a	RCA, LCX	No	-
	37 (1)	F	Hypertension,	High	RCA	No	-
			smoking
Ioannides et al [11]	42 (1)	M	Obesity, type 2 diabetes	High	LAD	NO	MI, nonsustained VT
Bogaz et al [1]	45 (1)	F	Hypertension,	High	RCA	NO	nonsustained VT
Current case	37	M	smoking Smoking	High a	RCA/LAD	No	-

15 minutes. The patient was transferred to the intensive care coronary unit. Three sets of troponin T levels and creatine kinase values were negative. Repeated coronary angiography revealed patent epicardial coronary arteries (Fig. 3). The patient was kept on oral calcium channel blocker, nitrate, statin, and aspirin orally. No further chest pain has been reported during his follow-up.

We report a young male patient who developed chest pain and STE during DBS with no evidence of acute myocardial infarction; and subsequently, coronary angiogram revealed patent epicardial vessels. Electrocardiographic change with STE during DBS is uncommon and is almost always associated with prior myocardial infarction, significant coronary artery disease, or transient total coronary occlusion. Dobutamine-induced STE in the absence of significant coronary artery disease is a rare condition and is supposed to be a consequence of severe coronary artery spasm [4-6]. Table 1 summarizes the published case reports for dobutamine-induced STE in patients with or without significant coronary artery lesions [1,4-11]. It is interesting to note that the pharmacodynamic action of dobutamine in the coronary arteries is primarily vasodilatation, which occurs because of ?2-adrenergic receptors stimulation in the presence of normofunctioning vascular endothelium [1]. Dobutamine binds not only to ?-1 receptors but also to ?-2 receptors and slightly stimulates ?-1 receptors. ?-Receptors play a role in exercise-induced coronary spasm. The augmentation of ?-1 stimulation in the presence of endothelial dysfunction induced by dobutamine may be related to the occurrence of coronary spasm [5]. Cigarette smoking, which is associated with endothelial dysfunction induced by free radicals, is a major risk factor for coronary spasm [12]. Kawano et al and others analyzed the response to a dobutamine infusion in patients with coronary arteries without angiographic lesions but with endothelial dysfunc- tion; the investigators demonstrated that, in 13% of these patients, angina with STE, preceded by changes in contractility on echocardiogram, was due to vasospasm by dobutamine [2,3,5]. Coronary artery spasm induced during DBS is a relatively rare finding with favorable short-term prognosis, and it may explain some of the erroneously classified “false-positive” examinations [3]. Moreover, intraventricular or left ventricular outflow gradients after dobutamine stress echocardiography have been reported. The left ventricular outflow obstruction may be related in part to the intense adrenergic stimulation during DBS. There are few reports of an association between dobutamine infusion and the development of takotsubo cardiomyopathy [13-15].

In conclusion, dobutamine stress echocardiography is a

reliable method to evaluate patients with a history of chest pain. However, serious complications should be anticipated during this test. Therefore, DSE is not a completely innocent method for diagnosing coronary artery disease because serious adverse events may occur albeit at a very low absolute rate. Guidelines of the American Heart Association

and the American College of Cardiology reported that stress pharmacologic challenge is sensitive and specific for detecting inducible ischemia in patients with moderate to high probability of disease with a reasonable degree of safety but not necessarily equally safe, considering DBS the least safe stress test [16].

Hesham Hussein MBchB, MD Department of Cardiology and Cardiovascular Surgery Hamad General Hospital, PO Box 3050

Doha, Qatar

Ayman El-Menyar MBchB, MSc

Weill Cornell Medical College

Doha, Qatar

Emad Ahmed MBchB, MD Department of Cardiology and Cardiovascular Surgery Hamad General Hospital, PO Box 3050

Doha, Qatar

Abdulrazzak Gehani MBchB

Weill Cornell Medical College

Doha, Qatar Department of Cardiology and Cardiovascular Surgery Hamad General Hospital, PO Box 3050

Doha, Qatar E-mail address: [email protected]

doi:10.1016/j.ajem.2010.04.012

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