Summary
Background
Non-invasive methods allow the evaluation of structural and functional arterial abnormalities. So far, no study has focused on the comparison of vascular parameters by type of cardiovascular event.
Methods
In this pilot study, cardiovascular risk factors, carotid parameters, carotid-to-femoral pulse wave velocity (PWV), brachial flow-mediated dilation and ambulatory blood pressure were assessed in patients who presented with acute coronary syndromes (ACS) or ischaemic atherothrombotic stroke (IAS). Groups were matched for age and gender.
Results
Prevalences of hypertension, diabetes and dyslipidaemia and heredity, smoking and body mass index were similar in the ACS ( n = 50) and IAS ( n = 50) groups. Carotid intima-media thickness (IMT) and PWV were significantly higher in the IAS vs. ACS group (769 ± 180 vs. 701 ± 136 μm; P = 0.039 and 12.5 ± 3.5 vs. 10.7 ± 2.4 m/s; P = 0.006). Carotid distensibility was significantly lower in the IAS vs. ACS group (16.2 ± 3.2 vs. 18.9 ± 7.6 10 −3 /kPa; P = 0.02). These differences persisted after adjustment for blood pressure for carotid distensibility but not for PWV. The prevalences of endothelial dysfunction and carotid plaques were not significantly different in the ACS and IAS groups (86% and 74%; 80% and 78%). In a multivariable model, carotid distensibility remained associated with ACS (odds ratio 1.19; 95% confidence interval 1.03–1.38; P = 0.016).
Conclusions
Stiffness and carotid wall thickness were higher in IAS than in ACS patients. These differences may support the interest in new therapeutic targets for cardiovascular secondary prevention.
NCT No
Résumé
Contexte
Des méthodes non invasives permettent maintenant d’évaluer les anomalies structurelles et fonctionnelles des artères. Aucune étude à ce jour n’a comparé ces anomalies selon l’événement athérothrombotique aigu.
Méthodes
Dans une étude pilote, les facteurs de risque cardiovasculaires, les paramètres carotidiens, la vitesse de l’onde de pouls (VOP), la dilatation de l’artère humérale médiée par le flux et la pression artérielle (PA) ambulatoire ont été évaluées chez patients qui ont présenté soit un syndrome coronarien aigu (SCA) ou un accident vasculaire cérébral (AVC) ischémique athérothrombotique (AVC), appariés pour l’âge et le sexe.
Résultats
La prévalence de l’hypertension artérielle, le diabète, la dyslipidémie, l’hérédité, le tabagisme et l’indice de masse corporelle étaient similaires dans les SCA ( n = 50) et AVC ( n = 50) groupes. L’épaisseur intima-média carotidienne (EIM) et la VOP étaient significativement plus élevée dans le groupe AVC vs SCA (769 ± 180 vs 701 ± 136 μm ; p = 0,039 et 12,5 ± 3,5 vs 10,7 ± 2,4 m/s ; p = 0,006). La distensibilité carotidienne (DC) était significativement plus faible dans le groupe AVC vs SCA (16,2 ± 3,2 vs 18,9 ± 7,6 10 −3 /kPa ; p = 0,02). Cette différence persistait pour la DC après ajustement pour la PA moyenne, mais pas pour la VOP. Les prévalences de la dysfonction endothéliale et des plaques carotidiennes n’étaient pas significativement différent dans les SCA et AVC groupes (86 % vs 74 % et 80 % vs 78 %). En analyse multivariée, DC restait associée à la survenue d’un SCA (rapport de cotes 1,19 ; 95 % intervalle de confiance 1,03–1,38 ; p = 0,016).
Conclusions
Chez les patients victimes d’un AVC ischémique athérothrombotique, la rigidité et l’épaisseur de la paroi carotidienne était plus élevé que chez les patients victime d’un SCA. Ces différences peuvent indiquer l’intérêt potentiel de nouvelles cibles thérapeutiques dans la prévention secondaire cardiovasculaire.
NCT n o
Background
Vascular, cerebral and cardiac events are major causes of morbidity and mortality in industrialized countries. Whereas acute coronary syndromes (ACS) are primarily due to coronary atherothrombosis, most ischaemic strokes are caused by carotid atherosclerosis and emboligenic cardiopathy. Many cardiovascular risk factors can promote the development of atherosclerosis, and their distribution differs by disease type. Thus, hypertension is more common in patients with stroke whereas smoking and dyslipidaemia are more marked in patients with coronary disease .
During the evolution of atherothrombotic disease, the arteries undergo modifications in their structure and function. These modifications, which can be analysed using non-invasive techniques, could play a part in the rupture of the plaque, which is responsible for the acute cardiovascular event. Laurent et al. demonstrated, in a longitudinal study, that an increase in arterial stiffness was an independent predictive factor for fatal stroke in 1715 patients with essential hypertension. To the best of our knowledge, no study has yet analysed arterial damages after the occurrence of an acute vascular event, comparing ischaemic atherothrombotic stroke (IAS) with ACS. The main objective of this study was to compare functional and structural arterial properties in patients who experienced two different consequences of a single disease (i.e. atherothrombosis): IAS and ACS. The hypothesis was that patients in the two groups differ in terms of arterial damage, with various cardiovascular risk factors.
Methods
Design and participants
This was a pilot, comparative, single-centre study conducted at Grenoble University Hospital. Male and female patients aged 40–70 years (to avoid selection of a particular atherothrombotic profile) who had presented with a completed IAS or ACS were included. Patients in the two groups were matched for age and gender. Inclusions were performed with a prospective sample of five patients in the same age range (± 5 years) and gender for each group. Age- and gender-matched patients without a history of acute cardiovascular events constituted a control group.
Exclusion criteria were:
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for patients in the ACS group: stroke within the previous 6 months (to decrease the role of acute biological and vascular modifications occurring at the initial phase of these two atherothrombotic events) or coronary bypass performed between the beginning of hospitalization for ACS and inclusion;
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for patients in the IAS group: cardioembolic disease (diagnosis left to the assessment of the neurologist having treated the stroke) or ACS within the previous 6 months;
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for all the patients: haemodynamic instability, atrial fibrillation or flutter, frequent extrasystoles (> 10/minute) (to obtain valid 24-hour ambulatory blood pressure blood pressure monitoring [ABPM]) and reduced mobility preventing the patient from maintaining a standing position.
When a patient was admitted in the emergency department at the hospital, their personal and family history was recorded, along with their cardiovascular risk factor profile and concomitant treatment. All patients underwent a physical examination at inclusion, including cardiovascular and neurological examinations, weight, height, abdominal circumference, systolic blood pressure (SBP) and diastolic blood pressure (DBP), heart rate measurement in accordance with European guidelines on treating hypertension and an electrocardiogram (ECG). At the time of the vascular event, when the patient was admitted in the emergency department at the hospital, all patients underwent a fasting blood sample for the measurement of lipid parameters, creatinine, insulin (no patients were treated with insulin) and glucose and, for those in the ACS group, an echocardiogram. In the 48 hours after the acute event, transthoracic and/or transoesophageal echocardiographies were performed for the IAS group, and all patients provided urine samples for the measurement of albuminuria over a 24-hour period. For both groups, a 24-hour ABPM (Spacelabs 90207 ® , Redmond, WA, USA) was performed after a ‘usual period’ of hypertension post-stroke (1 week after the acute event). The vascular examinations (carotid parameters, pulse wave velocity and endothelial function) were performed at 9 ± 2 days after acute events.
Ethical approval was obtained from the local ethics committee and all patients gave their written informed consent. The registration (ClinicalTrials.gov) trial number for this study is NCT00926874 .
Diagnosis of IAS and ACS
A diagnosis of IAS was made on the basis of patient interview data, physical examination and imaging tests (computed tomography [CT] scan and/or magnetic resonance imaging [MRI]) in the absence of haemorrhage but with direct signs of ischaemia. Conventional neurological tests (ultrasound of the supra-aortic arteries, ECG monitoring, cardiac ultrasound) were used to identify an atherothrombotic mechanism. An atherothrombotic mechanism was defined by:
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the presence of atherosclerotic thrombosis or stenosis (≥ 50% diameter reduction defined by the North American Symptomatic Carotid Endarterectomy Trial [NASCET] method and spectral Doppler ultrasound or < 50% but with plaque ulceration defined as an indentation, fissure or erosion on the luminal surface by long- and short-axis B-mode images ) in the clinically relevant extracranial or intracranial artery;
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the absence of acute cerebral infarction in a vascular territory other than the one of the stenosed or occluded artery;
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the absence of argument for another mechanism, particularly because of normal 48-hour ECG monitoring, normal transthoracic and transoesophageal echocardiography and absence of coagulopathy.
Patients with an arterial disease other than atherosclerosis (i.e. arterial dissection, vasculitis, arterial spasm) were excluded, as were patients who presented a lacunar stroke. These criteria were inspired by the Causative Classification System, which is an evidence-based classification algorithm for acute ischaemic stroke .
An ACS with persistent ST-segment elevation was diagnosed on the basis of patient interview data, ECG with signs of acute myocardial ischaemia and coronary angiography.
Evaluation of the structural and functional properties of the carotid artery wall
The two carotid arteries were studied successively by ultrasonography in mode B using a HP Sonos 2500 ® ultrasonic scanner (Hewlett-Packard ® , CA, USA), equipped with a 7.5 MHz sector probe. Carotid internal diameter was measured in two-dimensional mode in diastole (minimum diameter) and systole (maximum diameter) at 20 mm upstream of a carotid bifurcation. The stiffness (β) index was calculated for both common carotid arteries (CCAs). The β index was calculated using the formula:
β index = ln SBP/DBP /S
S = Ds − Dd /Dd
Carotid distensibility = 2 × Δ D / Dd / pulse pressure / 10 × 1.33 × 100
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