European Heart Journal Advance Access originally published online on December 16, 2005
European Heart Journal 2006 27(4):499-500; doi:10.1093/eurheartj/ehi690
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Dipyridamole echocardiography test in patients with normal or near normal coronary arteries: reply
CNR, Institute of Clinical Physiology
Via G. Moruzzi, 1
56124 Pisa
Italy
Tel: +39 050 3152397
Fax: +39 050 3152374
E-mail address: rosas{at}ifc.cnr.it
CNR, Institute of Clinical Physiology
Via G. Moruzzi, 1
56124 Pisa
Italy
We thank Dr Martínez-Sellés for the interest in our work and on the very appropriate comment focusing on this important issue, i.e. the potential correlation of coronary vasospasm in determining true ischaemia and wall motion abnormalities in patient with angiographically non-significant coronary artery disease. It is well known for 20 years that aminophylline administration may trigger coronary vasospasm in about one-third of patients with variant angina.1 The patient population under investigation pooled together subjects with different clinical conditions and heterogeneous angiographic patterns. Patients with variant angina were also enrolled in the study (the vasodilating stress test is used in this set of patients to exclude significant forms of coronary artery disease) but none of the patients experienced coronary vasospasm after aminophylline infusion. Moreover, none of the patients in our study with a positive test experienced an ST-segment elevation during dipyridamole infusion (prior to aminophylline infusion), indicating the presence of coronary vasospasm. However, as Martínez-Sellés correctly points out, there have been anecdotal reports of coronary vasospasm—documented by simultaneous electrocardiographic monitoring—occurring at the end of dipyridamole testing in patients subsequently shown to have variant angina. Nonetheless, the occurrence of this event is very uncommon and it is unlikely to have occurred in the patient population under investigation.
In our opinion, the results of the study by Fujita et al.,2 describing reversible perfusion abnormalities during dipyridamole stress in patients with variant angina and normal or near-normal coronary arteries are not consistent with vasospasm occurrence. In fact, 14 out of 16 patients had history of hypertension (n=5), and/or diabetes mellitus (n=2), and/or hypercholesterolaemia (n=9). All these factors are well-established causes of altered microcirculation as evidenced by perfusion scintigraphy and/or coronary flow reserve studies.3,4 In the same patient population, authors could not demonstrate a significant agreement between the presence of a perfusion defect and the angiographic site of coronary vasospasm, indicating that the altered coronary flow reserve could be attributed to other causes. In their conclusions, the authors state that perfusion defects are due to a concomitant microvascular dysfunction in patients with variant angina. In this particular case, we can evoke the ‘alternate’ or ‘inverse’ ischaemic cascade3 which refers to a sequence of clinical events during which the occurrence of wall motion abnormalities usually cannot be proved in spite of frequent occurrence of chest pain and ST-segment depression, although in a subset of patients, a reduction in coronary flow reserve and/or a metabolic evidence of inducible ischaemia has been described.
In more general terms, we certainly agree with Dr Martínez-Sellés that coronary vasospasm does exist, and it is a pivotal, often clinically unrecognized, mechanism underlying virtually all forms of ischaemic heart disease, from stable angina to unstable angina to acute myocardial infarction and sudden death. The landmark studies of coronary vasospasm were performed in the Institute of Clinical Physiology by Professor Attilio Maseri5 in the seventies. After 30 years, we certainly did not forget the Maseri lesson, and we agree with Martínez-Sellés that the single most important factor affecting the frequency with which variant angina is recognized depends on the physician's awareness of its existence. However, it is also true that it is not enough to be aware of coronary vasospasm to detect it.
The occasional occurrence of coronary vasospasm during dipyridamole infusion and the absence of clear-cut signs of coronary spasm exclude, at least in our patient population, a significant role of coronary vasospasm in the prognostic power of stratification of a positive stress echo with normal coronary arteries.
References
- Picano E, Lattanzi F, Masini M, Distante A, L'Abbate A. Aminophylline termination of dipyridamole stress as a trigger of coronary vasospasm in variant angina. Am J Cardiol 1988;62:694–697.[Medline]
- Fujita H, Yamabe H, Yokoyama M. Dipyridamole-induced reversible thallium-201 defect in patients with vasospastic angina and nearly normal coronary arteries. Clin Cardiol 2000;23:24–30.[Medline]
- Picano E, Palinkas A, Amyot R. Diagnosis of myocardial ischemia in hypertensive patients. J Hypertens 2001;19:1177–1183.[CrossRef][Web of Science][Medline]
- Dimitrow PP, Galderisi M, Rigo F. The non-invasive documentation of coronary microcirculation impairment: role of transthoracic echocardiography. Cardiovasc Ultrasound 2005;3:18.
- Maseri A, L'Abbate A, Baroldi G, Chierchia S, Marzilli M, Ballestra AM, Severi S, Parodi O, Biagini A, Distante A, Pesola A. Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of ‘preinfarction’ angina. N Engl J Med 1978;299:1271–1277.[Abstract]
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