Estelle Vautrin

First magnetic resonance coronary artery imaging of bioresorbable vascular scaffold in-patient

A 39-year-old man, active smoker with a history of hypercholesterolaemia, was referred for invasive coronary angiography for ST-segment elevation acute coronary syndrome. Coronary angiogram showed complete occlusion of the left anterior descending artery (LAD). Thromboaspiration was successfully performed with TIMI 3 flow at the end of the procedure. Therefore, no stenting procedure was immediately performed, and a control coronary angiography was performed …

Aortic Expansion Assessed by Imaging Follow-up after Acute Aortic Syndrome: Effect of Sleep Apnea

After surgical treatment of type A acute aortic syndrome (AAS), some patients exhibit aneurysmal aorta expansion (AAE) either upstream or downstream of the prosthetic tube. The mechanisms promoting AAE are not fully understood. It is recognized that intermediary mechanisms involved in obstructive sleep apnea (OSA) pathophysiology affect thoracic aorta expansion. The thoracic aorta of a patient with OSA is continuously strained by repetitive surges in blood pressure, transmural stretching resulting from huge variations in intrathoracic pressure, and intermittent hypoxiarelated vascular remodeling (1–4). To date, there are no data available on the effect of OSA on AAE after surgery for type A AAS. We retrospectively analyzed 62 patients initially surgically treated for type A AAS who were prospectively followed up by computed tomography or magnetic resonance imaging at 3 and 6 months postsurgery, and annually thereafter. At the 3-year median-term follow-up visit, the maximum rate of aortic diameter expansion (V : maxAo) was calculated to detect patients with stable aortic aneurysm or AAE. Patients with surgical or radiologic intervention on downstream aorta and Marfan syndrome were excluded. Independent observers, blinded to the clinical data, analyzed aortic images. V : maxAo was calculated as follows: (D22D1)/T, with D1 being the initial diameter and D2 the final diameter (maximum increase at the same anatomical level) between the first and the most recent postoperative measurements. The normal aortic expansion rate is 1 to 2 mm/yr (5). We classified patients into two groups: group 1, with no abnormal increase in aortic diameter (V : maxAo, 2 mm/yr), and group 2, for whom V : maxAo> 2 mm/yr. At the 3-year visit, all patients underwent 24-hour blood pressure monitoring (ABPM), biological assays, carotid-to-femoral pulse wave velocity measurement, and full polysomnography and answered the Epworth sleepiness scale questionnaire. SA was defined by an apnea–hypopnea index above 5 per hour of sleep and was considered central when more than 50% of apneas and hypopneas were central. All patients gave informed consent to participate in this institutional review board–approved study. The patients had undergone the following operations: replacement of the ascending aorta with an interposition tube graft (35 patients), of the ascending aorta and the aortic arch (5 patients), and of the ascending aorta and aortic valve by a composite graft (Bentall technique, 21 patients), and one patient had an interposition graft with separate aortic valve replacement. Table 1 summarizes the general characteristics of the study population that were similar for the two groups with the exception of the polysomnographic parameters. The prevalence of OSA was 72% throughout the population, and 18% of the patients presented with central SA. The prevalence of central SA and OSA was similar in patients with or without AAE (15% vs. 19% and 70% vs. 74% [P = 0.6], respectively). However, hypoxia during sleep was worse in patients with AAE, who had a significantly lower mean nocturnal SpO2 than those without AAE (92.56 1.9 vs. 93.66 1.7; P, 0.04) (Figure 1). The Epworth sleepiness score was 5.66 4.9 in patients without AAE and 7.16 5.6 in patients with AAE (P = 0.39). The prevalence of office hypertension (BP values. 135/80 mm Hg) was 77%, with 40% of patients exhibiting resistant hypertension. Using ABPM, 44% of patients had 24-hour hypertension, 42% had daytime hypertension, and 57% had nighttime hypertension. The prevalence of office and 24-hour ABPM hypertension was similar in both groups. The baseline aortic dimensions did not influence secondary dilatation (r = 0.11; P = 0.6). In patients with increasing aortic diameter, V : maxAo was significantly correlated with 24-hour systolic BP (r = 0.374; P = 0.013) and mean nocturnal SpO2 (r =20.381; P = 0.02). On multivariate analysis, the V : maxAo was independently (adjusted for age, body mass index, creatinine level) and positively correlated with mean nocturnal SpO2 (b =20.479; P = 0.01). In multivariate logistic regression analysis, only mean nocturnal SpO2 was independently (adjusted for the same parameters) and significantly predictive of absence of AAE (odds ratio = 0.549; 95% confidence interval, 0.35–0.862; P = 0.009). Figure E1 in the online supplement shows images in a patient who presented with severe OSA and AAE. Our original data set demonstrates the high prevalence of SA in patients with surgical procedures for type A AAS. Our study demonstrates a positive association between AAE and SA severity, as assessed by the degree of intermittent hypoxia. To date, only one study has reported the prevalence of OSA in patients who presented AAS. Sampol and colleagues compared 19 patients with a history of operated type A or medically treated type B aortic dissection with 19 hypertensive patients without aortic disease (6). They found that patients with aortic disease more frequently suffered from severe OSA than patients with hypertension. However, this case–control study did not permit us to clarify whether SA is a risk factor for AAE and was not designed to evaluate deterioration in patients with aortic disease. Here we used a retrospective study that included, by design, some limitations. We show the deleterious role of SA-linked intermittent hypoxia on the evolution of aortic diameters. We have previously described the deleterious role of hypoxia that increases carotid (7) and aortic (8) root diameters in patients with OSA. Nocturnal hypoxia increases sympathetic activity. Supported by the French Society of Hypertension and the Clinical Research Department at Grenoble University Hospital.

Hemorrhagic tamponade due to cardiac angiosarcoma.

Prognosis of angiosarcoma, the most common primary malignant cardiac tumor, is very poor. An early detection and treatment may extend survival beyond one year. Newer imaging modalities, including magnetic resonance imaging (MRI), play an important role in the evaluation of cardiac masses. The case of a man admitted to the emergency room for a cardiac tamponade is reported. Thoracic computed tomography and MRI diagnosed a pericardial tumor, for which surgical biopsy revealed an angiosarcoma. Chemotherapy was started, and the patient survived for 28 months. Etiologies of hemorrhagic tamponades are discussed, as well as treatment of cardiac angiosarcoma.

SPECT myocardial ischemia in the absence of obstructive CAD: Contribution of the invasive assessment of microvascular dysfunction

Coronary microvascular dysfunction has recently emerged as a major independent prognostic factor and can be invasively assessed by coronary flow reserve (CFR) and the index of microvascular resistance (IMR). The incremental prognostic value of myocardial ischemia from SPECT myocardial perfusion imaging (MPI) over clinical characteristics, cardiac risk factors, and stress test data for the prediction of hard cardiac events (myocardial infarction and cardiac death) has been well demonstrated over the last two decades regardless of the absence or presence of epicardial CAD. Recently developed semi-conductor, cardiac-dedicated cameras allow for decreased acquisition times and systematic procubitus and decubitus acquisitions thereby limiting the occurrence of false positives historically attributable to artefactual motion, attenuation, and digestive artifacts. It is therefore likely that pathophysiological causes rather than acquisition artifacts might underlie SPECT perfusion abnormalities. Here, we report four representative examples of patients presenting with ischemia in the setting of no obstructive CAD and normal fractional flow reserve together with elevated IMR and low CFR. The results indicate that ischemia from SPECT MPI could result from microvascular dysfunction in patients without obstructive CAD and should be considered as a prognostic factor for hard cardiac events.

0005 : Prognostic value of myocardial perfusion SPECT without significant perfusion defect using a dual isotope protocol and a novel CZT camera: interim results of the PROMHETE study

Background New dedicated cardiac gamma cameras using CZT detectors have shown significant improvement over the Anger camera regarding physical parameters, and their diagnostic performances have been validated in clinical studies. To date, few studies have evaluated the prognostic value of a low to intermediate risk single-photon emission tomography (SPECT) myocardial perfusion imaging (MPI) with these cameras, and only one with a HSDI stress thallium-201/rest Technetium-99m protocol on a CZT camera. Methods The study included patients who had no or minimal perfusion defects ( Results 212 patients (37%) underwent exercise stress and 366 (63%) had pharmacological stress (of which 89% had dipyridamole and 11% had dobutamine). Mean summed stress score was 0.95±1.2 [0-5]. During the follow-up period 25 hard cardiac events occurred. Annualized event rate was 1.3%/y. In the subgroup of patients undergoing exercise stress test, annualized event rate was 0.43%/y. Multivariate Cox analysis identified age (HR 1.14 [1.08; 1.20], p Conclusions The use of a HS-DI protocol on a CZT camera provides prognostic information, comparable to single-isotope protocols on conventional Anger camera, while reducing imaging time and without increasing the injected activity. The author hereby declares no conflict of interest

Pulmonary Capillary Wedge Pressure Measurement: A Challenge for Diagnosis of Pulmonary Arterial Hypertension

Background: International registries report an aging population suffering from PAH (Pulmonary Artery Hypertension) engendering diagnosis difficulties linked with growing cases of group 2 related to left heart failure with preserved Ejection Fraction (PH-HFpE). Pulmonary Capillary Wedge Pressure (PCWP) measurement by right heart catheterization remains a technical challenge for patient classification; many centers still use digital PCWP given by cath lab software. Here, we have tried to demonstrate misclassification impact of this approximation. Methods: We investigated the PCWP-Left Ventricular End Diastolic Pressure (LVEDP) relationship in a prospective series of 31 patients undergoing heart catherization for suspicion of PAH. Digital and end expiration PCWP were measured in right and left pulmonary arteries for comparison with end expiration LVEDP. Results: We explored 31 patients, 65.4 ± 11 years old, 67.7% were female, with LVEF 60.6 ± 5.2%, Diagnosis of HFpEF was found in 62% of cases and PAH in 10% when using end expiration LVEDP. Right end expiration PCWP, left end expiration PCWP, right digital PCWP, left digital PCWP and end expiration LVEDP were respectively 16.2 ± 6.7mmHg, 16,6 ± 6.4mmHg, 12.2 ± 6.1mmHg (p<0.001), 12.7 ± 6.1mmHg, and 15.8 +/- 4.8mmHg, with a significant difference (p<0.001) between the right and left digital PCWP and end expiration LVEDP. Conclusion: Using digital PCWP instead of end expiration PCWP measurement during RHC, results in a significant underestimation of the LVEDP, this translated to 22% of patients with Pulmonary Hypertension (PH) being misclassified as having group1 rather than group2 PH. Misclassified patients are at risk of receiving inadequate therapy and biased therapeutic studies. When in doubt left heart catheterization should be performed for PAH diagnosis.