Multiple complex stenoses and chronic stable angina pectoris

Abstract

We read with interest the report by Kruk et al. [1]regarding angiographic and ultrasound coronary lesioncharacteristics in patients with chronic stable angina(CSA) pectoris. Kruk et al. showed that multiple complexlesions (N1 lesion) with vulnerable characteristics arepresent in nearly one third of patients with CSA. Thisfinding is important and consistent with previous worksuggesting a role of plaque complexity in the rapidprogression of stenosis in patients with stable coronaryartery disease.Kruk et al. state that b...no previous study assessed theprevalence of multiple complex lesions in patients withstable angina.Q Unfortunately, they were unaware of a recentstudy from our institution [2] regarding inflammatorymarkers and multiple complex stenoses in patients withCSA. Our study showed a high prevalence of complexlesions in patients with CSA pectoris. Among 121 patientswith significant stenoses, 37 (30.6%) had one complexlesion, 38 (31.4%) had multiple complex stenoses, and 46patients (38%) had no complex stenoses. Of interest, wealso assessed lesion complexity according to AHA/ACCclassification, and found that 88% of the complex stenoseswere type C.The Kruk et al. [1] paper confirms our previous findingsregarding the presence of multiple complex stenoses inpatients with CSA pectoris, and expands our previousangiographic observations. The authors analyse ultrasoundlesion characteristics—an issue not previously assessed bythe studies of ourgroup. Kruk et al.’s results are important asthey provide insight regarding plaque vulnerability inpatients with CSA pectoris—an issue that has been littleexplored previously. Both our study [2] and that of Kruk etal. [1] suggest that although increased atheromatous plaqueactivity is more common in patients with acute coronarysyndromes, clinical stability in patients with CSA pectorisdoes not necessarily indicate the absence of vulnerableatheromatous plaques. It has been shown that a sizeableproportion of plaques in CSA patients has inflammatoryfeatures and is prothrombotic. Coronary artery diseaseprogression leading to coronary artery occlusion and/oracute coronary events in patients with CSA pectoris isunpredictable. We have previously shown that complexstenoses are at a higher risk of progression than smoothlesions [3]. Although coronary stenosis progression isinfluenced by both local and systemic factors, the precisemechanisms underlying this process remain elusive. Inrecent years, it has become apparent that inflammatorymechanisms involved in atherogenesis may lead to plaquedisruption, stenosis progression, and acute coronary syn-dromes. A role has been suggested for systemic inflamma-tion in the genesis of coronary artery disease progression [4]and multifocal plaque disruption. Previous studies from ourgroup have shown that inflammatory markers correlate withthe number of complex lesions in patients with angina [5,6],supporting a role of inflammation in lesion complexity andplaque vulnerability.Of interest, a recent coronary intravascular ultrasoundstudy in 235 patients showed that multiple plaque ruptureswere observed in 20% of AMI and in 6% of stable anginapatients. In AMI patients, multiple plaque rupture wasassociated with a high CRP level, whereas in stable anginapatients, plaque rupture was more common in those withdiabetes [7].