[Emergent transcatheter aortic valve implantation in a patient with bicuspid aortic valve stenosis in cardiogenic shock]. / Choc cardiogénique sur bicuspidie aortique sténosante traité par remplacement valvulaire aortique percutané en urgence.

Transcatheter aortic valve implantation is a therapeutic option for high-risk patients with severe aortic valve stenosis and with cardiac symptoms. This procedure requires the preliminary evaluation by a "heart team" and presents some contraindications. We report the case of a 58-year-old man with severe bicuspid aortic valve stenosis and cardiogenic shock. In spite of contraindications and because of the failure of balloon aortic valvuloplasty, transcatheter aortic valve implantation was performed in emergency.

No post-conditioning in the human heart with thrombolysis in myocardial infarction flow 2-3 on admission.

AIMS: Proof-of-concept evidence suggests that mechanical ischaemic post-conditioning (PostC) reduces infarct size when applied immediately after culprit coronary artery re-opening in ST-elevation myocardial infarction (STEMI) patients with thrombolysis in myocardial infarction 0-1 (TIMI 0-1) flow grade at admission. Whether PostC might also be protective in patients with a TIMI 2-3 flow grade on admission (corresponding to a delayed application of the post-conditioning algorithm) remains undetermined. METHODS AND RESULTS: In this multi-centre, randomized, single-blinded, controlled study, STEMI patients with a 2-3 TIMI coronary flow grade at admission underwent direct stenting of the culprit lesion, followed (PostC group) or not (control group) by four cycles of (1 min inflation/1 min deflation) of the angioplasty balloon to trigger post-conditioning. Infarct size was assessed both by cardiac magnetic resonance at Day 5 (primary endpoint) and cardiac enzymes release (secondary endpoint). Ninety-nine patients were prospectively enrolled. Baseline characteristics were comparable between control and PostC groups. Despite comparable size of area at risk (AAR) (38 ± 12 vs. 38 ± 13% of the LV circumference, respectively, P = 0.89) and similar time from onset to intervention (249 ± 148 vs. 263 ± 209 min, respectively, P = 0.93) in the two groups, PostC did not significantly reduce cardiac magnetic resonance infarct size (23 ± 17 and 21 ± 18 g in the treated vs. control group, respectively, P = 0.64). Similar results were found when using creatine kinase and troponin I release, even after adjustment for the size of the AAR. CONCLUSION: This study shows that infarct size reduction by mechanical ischaemic PostC is lost when applied to patients with a TIMI 2-3 flow grade at admission. This indicates that the timing of the protective intervention with respect to the onset of reperfusion is a key factor for preventing lethal reperfusion injury in STEMI patients. CLINICAL TRIAL NUMBER: NCT01483755.

[Platypnea-orthodeoxia syndrome: case report]. / Le syndrome de platydéoxie-orthopnée : à propos d'un cas.

We report the case of an 80-year-old woman with symptomatic postural hypoxaemia caused by a right-to-left shunt through a patent foramen ovale. The hypoxaemia was enhanced by the supine position and disappeared in upright position. Potential mechanisms underlying postural variations of the shunt seemed to be similar to those describe in platypnea-orthodeoxia syndrome. Patient became asymptomatic after shunt resolution.

A novel minimal invasive closed chest myocardial ischaemia reperfusion model in rhesus monkeys (Macaca mulatta): improved stability of cardiorespiratory parameters.

The aim of this study was to report the cardiorespiratory events observed during coronary artery occlusion and reperfusion in a minimally invasive closed chest myocardial occlusion-reperfusion model in rhesus monkeys. We hypothesized that a minimally invasive technique may lead to fewer cardiac arrhythmias and complications. Eight male rhesus macaques 10-15 kg and 10-15 years old were sedated with ketamine (2 mg/kg), midazolam (1.3 mg/kg), atropine (0.01 mg/kg) and buprenorphine 0.02 mg/kg intramuscularly. Etomidate 1-2 mg/kg was injected intravenously to allow tracheal intubation. Anaesthesia was maintained with isoflurane. Pulse oximetry, electrocardiogram (ECG), heart rate, mean arterial blood pressure (MAP), inspired isoflurane fractions (F(I)ISO) and core temperature were recorded every 10 min. The coronary artery occlusion was induced by a balloon-tipped catheter advanced via the femoral artery into the left anterior descending artery and inflated to completely occlude the vessel for 20-50 min (IT) before reperfusion. Sequences of elevated ST segment, QRS complex prolongation, ventricular premature complexes and ventricular fibrillation were observed with a lower incidence than previously described in the literature. IT was (min: 17; max: 50) min long. F(I)ISO was lower than the minimal alveolar concentration in these species. Hypotension (MAP < 70 mmHg) and hypothermia (T°C < 36°C) were observed in all macaques. This minimally invasive closed chest model was successful in providing better cardiorespiratory physiological parameters than reported in previous models. The benefit (achieving ischaemia) versus risk (lethal arrhythmia) of the duration of the coronary occlusion should be considered.

Acute stroke and heart attack management within a four-hour time window.

BACKGROUND AND PURPOSE: Although brain embolism is a uncommon complication of myocardial infarction, sequential treatment of cerebral and coronary artery occlusion within a 4-hour time window is unusual. SUMMARY: of case A 60 year-old man experienced successful intravenous recombinant thrombolysis (tPA) for acute middle cerebral artery (MCA) occlusion followed by efficient angioplasty stenting of a troponin-negative coronary occlusion which, while painless, involved clear electrocardiographic abnormalities. Both pathologies were treated within a 4-hour time window. CONCLUSION: Acute brain and heart ischemia may be successfully treated within a 4-hour time window, thanks to an efficient multidisciplinary approach.

Reliability and limitations of angiography in the diagnosis of coronary plaque rupture: an intravascular ultrasound study.

OBJECTIVE: Intravascular ultrasound (IVUS) is a cornerstone tool for the diagnosis of plaque rupture (PR) but is usually used secondary to the suspicion of PR on angiography; the true incidence of PR may therefore be overestimated. We sought to evaluate predictors of angiographic diagnosis of PR using a non-angiographically driven IVUS examination. METHODS AND RESULTS: Diagnosis of PR on IVUS required agreement between two operators blinded to the results of angiography. Any irregular lesion with ulceration, flap or aneurysm on a qualitative angiogram was considered suspicious for PR. IVUS-detected PR and non-PR lesions were compared with the corresponding angiograms. A total of 224 distinct (ruptured or non-ruptured) lesions were detected by IVUS in 65 patients; 49 of the 105 IVUS-detected non-culprit PRs were suspected on angiography. The positive and negative predictive values for correct angiographic diagnosis of PR were 96% and 61%, respectively. Proximal coronary location, wide cavity, and counterflow rupture were strong predictors of correct angiographic diagnosis, enabling four specific angiographic patterns to be identified using three-dimensional IVUS PR reconstruction. CONCLUSION: Against IVUS as the gold standard, angiographic diagnosis of PR showed good specificity but low sensitivity. However, better angiographic diagnosis should enable medical treatment to be optimized, especially with respect to statin therapy.

Morphological and biomechanical aspects of vulnerable coronary plaque.

Vulnerable plaque morphology has been described by gross pathology and intravascular ultrasound, but morphological criteria cannot fully explain vulnerability, which involves four distinct factors: 1) inflammatory and biological processes; 2) geometry; 3) composition; and 4) hemodynamic stress. These last three aspects underlie the biomechanical study of vulnerable plaque. By virtue of the nature of their evolution, atherosclerotic plaques tend to be excentric, and this is a crucial morphological feature, causing circumferential stress to peak in very specific juxta-luminal locations, where it can exceed the rupture threshold of collagen, the basic constituent of arterial architecture. The lipido-necrotic core covered by a fibrous cap, formed in young plaques, is another morphological feature, which, can also increase and concentrate circumference stress in the juxta-luminal fibrous cap. The larger the lipid core, the thinner the fibrous cap and the greater is the stress. There are also inflammatory processes in such areas, which tend to reduce cap thickness. Ruptures occur when this thickness falls below 65 microns. Heart rate, blood pressure and pulse pressure are all biomechanical factors affecting vulnerable arterial walls, increasing circumferential stress and material fatigue. Vulnerable plaques are almost always associated with positive arterial remodeling. Numerical simulation has shown such so-called compensatory remodeling to be exclusively due to the healthy arc stretching in vulnerable plaques. Positive remodeling is optimal when the healthy arc is around 170 degrees, which keeps the lumen area relatively stable as long as the plaque does not exceed 40% to 50%. This mechanism does not apply to concentric plaques. In conclusion, the mechanism of vulnerable plaque rupture is highly complex and multifactorial. This complexity more or less precludes prediction in individual cases: we are in the realms of chaos theory and acute sensitivity to initial conditions. The greatest caution is therefore required in any attempt to predict rupture from diagnostic imagery, which provides only morphological data on plaque's nature.

[Myocardial bridging and coronary spasm on effort]. / Pont myocardique et spasme coronaire à l'effort.

The discovery of myocardial bridging during coronary angiographies is common. Yet these bridges are rarely the origin of acute coronary syndrome. We report the case of an active 45 year old man with no cardiovascular risk factors who had acute coronary syndrome. Emergency coronary angiography just revealed two myocardial bridges on the anterior interventricular artery which did not explain this acute episode. A subsequent second angiogram together with endocoronary echography demonstrated that there was no atheroma and a methergin test set off diffuse coronary spasm. The association of myocardial bridging and coronary spasm has only rarely been reported in the literature. We describe the clinical, therapeutic and prognostic characteristics.

[Morphological and functional characteristics of the culprit coronary artery in acute coronary syndrome]. / Aspects morphologiques et fonctionnels de l'artère coronaire coupable d'un syndrome coronaire aigu.

In the catheter laboratory, faced with a patient with unstable angina, the problem is not the diagnosis of epicardial coronary artery stenosis but rather the atherothrombotic complexity of the stenosis and the identification of other less stenotic lesions on angiographically normal or nearly normal segments. The authors describe two appearances with morphological analysis of the vulnerable or unstable plaque and functional analysis of coronary artery vasomotricity. Acute coronary syndromes due to a clearly stenotic atherothrombotic plaque on angiography pose no diagnostic problems. However, an acute coronary syndrome may be more difficult to assess when angiography shows only simple irregularities of the lumen or no lesions at all. In these cases, angiography is said to be normal and the coronary arteries are considered to be possibly "healthy". Evaluation of the vessels' vasomotricity is especially valuable in this context. Using pharmacological stress tests, endovascular ultrasonography is a complementary diagnostic tool which allows identification of the unstable atheromatous process or of a partial atherothrombosis masked by positive remodelling process. These tests may also indicate the optimal treatment.

Preconditioning during coronary angioplasty: no influence of collateral perfusion or the size of the area at risk.

AIMS: It is unclear whether the protection observed in human heart following repetition of brief episodes of ischaemia is due to opening of coronary collaterals or to ischaemic preconditioning. We investigated whether the improvement in ST segment change following repeated episodes of brief ischaemia during coronary angioplasty is due to preconditioning when the size of the area at risk and the collateral flow are taken into account. METHODS AND RESULTS: Thirty-six patients underwent percutaneous transluminal coronary angioplasty. Intracoronary ST segment changes were measured throughout the procedure and used as an endpoint. The size of the area at risk and the collateral perfusion within the ischaemic bed were measured using single photon emission computerized tomography (SPECT). Mean ST segment shift observed in all patients significantly decreased from 11.0+/-2.6 mm during the first balloon inflation to 8.5+/-2.3 mm during the second inflation. This protective effect occurred in the absence of any change in the size of the area at risk (mean: 46+/-5% of LV) and of the collateral perfusion to the ischaemic zone (mean: 23+/-4% of flow in the non-ischaemic zone). CONCLUSION: These results suggest that ischaemic preconditioning does occur during repeated brief coronary artery occlusion in the human heart.

[Sudden death by coronary spasm: a particular and often unrecognised clinical entity]. / Mort subite par s pasme coronaire: une entité particulière, trop souvent méconnue.

The authors report 3 cases of resuscitated sudden death in which the investigations clearly showed coronary spasm. This was demonstrated by systematic coronary angiography with an ergometric test. Two patients underwent electrophysiological investigations which were normal. The three patients were prescribed long-term calcium antagonist therapy and one of them underwent coronary angioplasty. With a follow-up of 6 months to 3 years, there was no clinical recurrence or documented arrhythmia. A review of the literature shows that this is a cause of sudden death which is probably underestimated and unrecognised. Electrophysiological investigations often give disappointing results and medical therapy is the keystone of treatment. Coronary angioplasty and implantation of an automatic defibrillator are second-line treatments reserved to forms refractory to medical therapy.

Experimental assessment of new stent technologies: validation of a comparative paired rabbit iliac artery study model.

Preventing coronary in-stent restenosis is a major challenge for physicians and industry. To assess new stent technologies, a comparative paired iliac artery model in rabbits is proposed. One tubular stent was implanted in each external iliac artery in 12 rabbits (i.e., 24 stents). An artery overdilatation level of 20% was strictly observed. Restenosis was examined at 30 days by angiography, intravascular ultrasound (IVUS) examination, and histomorphometry. On quantitative angiography, the mean loss of angiographic diameter was 9.8 +/- 4.4% in the right as compared to 9.3 +/- 55% in the left artery (p = 0.75). On IVUS, the volume of intrastent neointimal proliferation was 26.6 +/- 4.9 mm(3) in the right and 25.8 +/- 3.5 mm(3) in the left artery (p = 0.58). In histomorphometry, the neointimal proliferation area was 0.78 +/- 17 mm(2) in the right and 0.76 +/- 0.17 mm(2) in the left artery (p = 0.87). Intrastent neointimal proliferation was comparable between the left and right arteries of all rabbits. The model has three main advantages: (1) arterial dilatation and thus arterial wall aggression are controlled, (2) pairing makes each animal its own control subject, and (3) the statistical power for comparative testing is maximized. The model enables the effect of a new drug-delivery device to be assessed.

[Coronary pressure measurement for functional evaluation and treatment of intermediate angiographic stenosis]. / Apport des guides de pression intracoronaire pour l'évaluation fonctionnelle et le traitement des sténoses angiographiques intermédiaires.

Accurate understanding of the physiopathology of a coronary stenosis is a major objective in management during diagnostic coronary angiography. Measurement of fractional flow reserve (FFR) by coronary pressure measurement is a reliable method for evaluating the functional consequences of a lesion of the myocardium. This retrospective monocentric study of 114 patients showed that routine coronary pressure measurement for assessing the functional consequences of intermediate (30 to 70% stenosis) lesions or those of ambiguous topography: was necessary in 4% of diagnostic coronary angiographies enabling an immediate management decision. Using this method, 34% of complementary investigations were not performed (stress test, myocardial scintigraphy, dobutamine stress echocardiography). Seventeen per cent of unnecessary angioplasties were also avoided so that acute coronary event were also avoided when lesions with a FFR >0.75 were not treated by angioplasty. A 10-14% reduction in cost was achieved compared with a strategy of systematic angioplasty in respectively mono- or multivessel disease patients and 39% compared with performing ambulatory myocardial scintigraphy in patients with multivessel disease.

[Predictive value of glycemia in acute coronary syndromes]. / Valeurs prédictives de la glycémie dans les syndromes coronaires aigus. Revue de la littérature.

Intravenous insulin therapy is used in diabetic patients at the acute phase of coronary syndrome (ACS). However, hyperglycemia in diabetic patients is a powerful predictive factor for patient outcome as it is associated with a doubling of in-hospital mortality and poor long-term prognosis. Recent studies involving non-diabetic patients show that even mild hyperglycemia in the setting of ACS is also a predictive factor of in-hospital mortality. Moreover, the new entity called impaired fasting glucose (IFG) (6.1 to 7 mmol/L) is not only an independent factor of mortality for coronary patients, but very recently has also been associated with a doubling of the risk of in-hospital mortality in the setting of ACS. Admission as well as follow-up glycaemia are fundamental parameters in ACS on the one hand for their prognostic value, and on the other end as a diagnostic tool in determining the presence of diabetes or IFG.

Mechanism of lumen enlargement with direct stenting versus predilatation stenting: influence of remodelling and plaque characteristics assessed by volumetric intracoronary ultrasound.

OBJECTIVE: To compare the effects of arterial remodelling and plaque characteristics on the mechanisms of direct stenting and predilatation stenting. Direct stenting has become routine in some laboratories and differs technically from predilatation stenting. METHODS: Pre- and post-interventional volumetric intravascular ultrasound (IVUS) was undertaken in 30 patients with direct stenting and in 30 with predilatation stenting of non-calcified native coronary lesions, using the same stent design and stent length. Lumen, vessel (external elastic membrane (EEM)), and plaque (plaque + media) volumes were calculated. Remodelling was determined by comparing the EEM area at the centre of the lesion with the EEM areas at proximal and distal reference sites. Plaque eccentricity was defined as the thinnest plaque diameter to the thickest plaque diameter ratio. Plaque composition was characterised as soft, mixed, or dense. RESULTS: All volumetric IVUS changes were similar in the two groups. Pre-intervention remodelling remained uninfluenced after direct stenting, but was neutralised after predilatation stenting. Eccentric lesions responded to intervention by a greater luminal gain owing to greater vessel expansion in direct stenting. Plaque composition influenced luminal gain in direct stenting, the gain being greatest in the softest plaques; in predilatation stenting, luminal gain was equivalent but vessel expansion was greater for "dense" plaque and plaque reduction greater for "soft" plaque. CONCLUSIONS: In non-calcified lesions, the mechanisms of lumen enlargement after direct or predilatation stenting are significantly influenced by atherosclerotic remodelling, plaque eccentricity, and plaque composition.