1000–32 Spontaneous Evolution of Nonocclusive Coronary Dissection After PTCA: A 6 Month Angiographic Follow-up Study

We have previously shown that, when good distal flow is maintained, dissection after PTCA has a favourable short term (24 hrs) evolution and does not require bail-out interventions or CABG.To evaluate the long term (6 months) clinical and angiographic evolution of non occlusive dissection, we submitted 129 consecutive patients (103 male, mean age 53±11 yrs) undergoing elective PTCA (147 lesions, 66 LAD, 49 CX, 32 DX) to repeat angiography 24 hrs and 6 months after the procedure. Lesions were measured by QCA and coronary dissection was graded using the NHLBI classification (types A-E; Huber Am J Cardiol 1991;68: 467). Mean stenosis was 85±11% before and 25±7% immediately after PTCA (p<0.001). Residual stenosis was not significantly different at the 24 hrs restudy (24±9%). Non occlusive coronary dissection (flow TIMI grade 3 in all pts) was seen in 49/147 lesions (33%) and evolved as follows:Dissection (tot)Immediate 49 (33%)24 hrs 41 (28%)6 months 18 (12%)A332710B1085C442D221At the 6 month follow-up study, restenosis was seen in 51/147 lesions (34%), of which 5/49 (10%) had dissection and 46/106 (43%) did not. No cardiovascular events or recurrence of symptoms were recorded in the absence of restenosis.Therefore 1) nonocclusive dissection after PTCA usually improves after 6 month; 2) in the absence of flow impairment and ischemia this complication does not require any further intervention; 3) non occlusive dissection is not associated with increased incidence of restenosis

A Unique Case of Mitral Valve Double Papillary Muscle Rupture

Abstract Papillary muscle rupture is a rare and life-threatening complication of acute myocardial infarction (AMI). We present a unique case of double papillary muscle rupture in a patient with three vessel disease and acute thrombotic occlusion of left circumflex obtuse marginal artery as the culprit lesion. (Level of Difficulty: Beginner.

Energy cost of walking with hip joint impairment

The energy cost of walking was measured in 12 patients (age 39-73 years) with hip joint impairment and 10 healthy controls during unassisted walking (2-6 km\ub7h -1) on a level treadmill surface and on a 5% incline. The energy cost of locomotion in most patients increased up to 50% and 70% during level-surface and uphill walking, respectively. This difference between patients and controls was probably due to the increased external mechanical work. The energy cost of walking, although related to pain experienced during walking but not hip joint range of motion or to joint status evaluated radiographically, provides an additional variable when defining the conditions of disability and functional impairment individuals with this pathological condition

Impact of substitution among generic drugs on persistence and adherence: A retrospective claims data study from 2 Local Healthcare Units in the Lombardy Region of Italy

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MitraClip Treatment of Secondary Mitral Regurgitation in Heart Failure with Reduced Ejection Fraction: Lessons and Implications from Trials and Registries

Transcatheter mitral valve intervention using the MitraClip system has evolved as a new tool for the treatment of secondary mitral regurgitation (SMR) in patients with heart failure and reduced lef..

Gene expression profile of rat left ventricles reveals persisting changes following chronic mild exercise protocol: implications for cardioprotection

<p>Abstract</p> <p>Background</p> <p>Epidemiological studies showed that physical exercise, specifically moderate lifelong training, is protective against cardiovascular morbidity and mortality. Most experimental work has focused into the effects and molecular mechanisms underlying intense, rather than mild exercise, by exploring the acute effect of training. Our study aims at investigating the cardioprotective effect of mild chronic exercise training and the gene expression profile changes at 48 hrs after the exercise cessation. Rats were trained at mild intensity on a treadmill: 25 m/min, 10%incline, 1 h/day, 3 days/week, 10 weeks; about 60% of the maximum aerobic power. By Affymetrix technology, we investigated the gene expression profile induced by exercise training in the left ventricle (LV) of trained (n = 10) and control (n = 10) rats. Cardioprotection was investigated by ischemia/reperfusion experiments (n = 10 trained vs. n = 10 control rats).</p> <p>Results</p> <p>Mild exercise did not induce cardiac hypertrophy and was cardioprotective as demonstrated by the decreased infarct size (p = 0.02) after ischemia/reperfusion experiments in trained with respect to control rats. Ten genes and 2 gene sets (two pathways) resulted altered in LV of exercised animals with respect to controls. We validated by real-time PCR the increased expression of four genes: similar to C11orf17 protein (RGD1306959), caveolin 3, enolase 3, and hypoxia inducible factor 1 alpha. Moreover, caveolin 3 protein levels were higher in exercised than control rats by immunohistochemistry and Western Blot analysis. Interestingly, the predicted gene similar to C11orf17 protein (RGD1306959) was significantly increased by exercise. This gene has a high homology with the human C11orf17 (alias: protein kinase-A interacting protein 1 or breast cancer associated gene 3). This is the first evidence that this gene is involved in the response to the exercise training.</p> <p>Conclusion</p> <p>Our data indicated that few, but significant, genes characterize the gene expression profile of the rat LV, when examined 48 hrs since the last training section and that mild exercise training determines cardioprotection without the induction of hypertrophy.</p

TCT-713 Impact And Evolution Of Right Ventricular Dysfunction After MitraClip In High Risk Patients With Functional Mitral Regurgitation

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Heart Failure With Mid-range or Recovered Ejection Fraction: Differential Determinants of Transition

The recent definition of an intermediate clinical phenotype of heart failure (HF) based on an ejection fraction (EF) of between 40% and 49%, namely HF with mid-range EF (HFmrEF), has fuelled investigations into the clinical profile and prognosis of this patient group. HFmrEF shares common clinical features with other HF phenotypes, such as a high prevalence of ischaemic aetiology, as in HF with reduced EF (HFrEF), or hypertension and diabetes, as in HF with preserved EF (HFpEF), and benefits from the cornerstone drugs indicated for HFrEF. Among the HF phenotypes, HFmrEF is characterised by the highest rate of transition to either recovery or worsening of the severe systolic dysfunction profile that is the target of disease-modifying therapies, with opposite prognostic implications. This article focuses on the epidemiology, clinical characteristics and therapeutic approaches for HFmrEF, and discusses the major determinants of transition to HFpEF or HFrEF

Partial persistence of exercise-induced myocardial angiogenesis following 4-week detraining in the rat

Enhanced angiogenesis, or capillary growth, has a prominent role among the various beneficial effects of exercise training on the myocardium. The aim of the present study is to assess if training-induced increases in capillarity and vascularization persist after 4 weeks of detraining. Adult male rats were trained to run on a treadmill for 10 weeks at approximately 60% VO(2max), which did not induce cardiac hypertrophy, but increased (P < 0.05) the soleus/body weight ratio, left ventricle capillarity and von Willebrand-positive cell density (n = 6). In another group of animals (n = 6) subjected to training followed by 4-week detraining, the soleus/body weight ratio returned to normal, with only partial reversal of left ventricle capillarity and von Willebrand-positive cell density. Markers of angiogenesis (VEGF, KDR/VEGF-R2 and HIF-1alpha mRNA, studied by real-time RT-PCR) were upregulated at the end of training, and returned to baseline value after detraining. Electron microscopy highlighted some morphological features in trained hearts (endothelial cell sprouting and bridges and pericyte detachment), suggestive of endothelial cell proliferation and capillary growth that were absent in untrained and detrained hearts. We conclude that the training-induced increase in cardiac capillarity and vascularization are retained for some time upon cessation of the training program even in the absence of angiogenic stimuli