While the disease course of stress-induced cardiomyopathy (SIC) is usually benign, it can be fatal in some cases. The prognostic factors to predict poorer outcome are not well established, however. We analyzed the Acute Physiology And Chronic Health Evaluation (APACHE) II score to assess its value for predicting poor prognosis in patients with SIC. Thirty-seven consecutive patients with SIC were followed prospectively during their hospitalization. Clinical factors, including APACHE II score, coronary angiogram, echocardiography and cardiac enzymes at presentation were analyzed. Of the 37 patients, 27 patients (73%) were women. The mean age was 66.1 ± 15.6 years, and the most common presentation was chest pain (38%). Initial echocardiographic left ventricular ejection fraction (EF) was 42.5 ± 9.3%, and the wall motion score index (WMSI) was 1.9 ± 0.3. Six patients (16%) expired during the follow-up period of hospitalization. Based on the analysis of characteristics and clinical factors, the only predictable variable in prognosis was APACHE II score. According to ROC curve by this result, we divided patients into two groups (APACHE II score > 20, and ≤20). The patients with APACHE II score greater than 20 had tendency to expire than the others (P = 0.001). Based on present study, APACHE II score more than 20, rather than cardiac function, was associated with mortality in patients with SIC.
Background: Up to the present, preload reduction in congestive heart failure (CHF) patients is performed with high potency diuretics. We reported in TCT/ACC 2014 and 2015, the hemodynamic changes of the first 6 CHF case in humans, using Percutaneous Transluminal Caval flow Restriction (PTCR) procedure achived with caval counterpulsation balloon (CCPB). This innovative method reduced preload in CHF. In this study we are reporting the results of the 6 consecutive patients with CHF, treated with intermittent preload reduction of caval flow with CCPB, guided by the respiratory phases. Now we are reporting the echocardiographic of these patients. Methods: 6 patients with CHF who met our protocol criteria, were evaluated. 4 were ischemic, and 2 non ischemic. The mean age was 58 ± 9. 4 male mean age 55 ± 6 years, and 2 female mean age 63 ± 4. We performed baseline Doppler echocardiography, coronary angiography and right heart catheterization. Subsequently caval flow restriction was started, through the right femoral vein, catheter balloon was introduced in the femoral vein and echo guided, placed just before hepatic vein drainage. The balloon was inflated according to previous calculations, to cover Inferior Vena Cava (IVC) remaining area completing 100% (total occlusion), and 70% during expiration (sub-occlusion), assuming 30% inspiratory collapse, resulting intermittent flow. The balloon was kept inflated for 30 minutes, right catheterization and echocardiography were repeated during inflated balloon. The balloon was removed and deflated. Results: Table. Echo Variables. Conclusion: We are reporting our echocardiography experience in 6 patients with CHF treated with intermittent reduction of preload with CCPB. Hemodynamic and echocardiographic changes obtained in these patients, suggest, that this innovative approach can play a role in the treatment of CHF patients.
Journal Article Is immunoperoxidase staining of endomyocardial biopsies for interstitial inflammatory cells helpful in the diagnosis of myocarditis? Get access J. F. Southern, J. F. Southern *Department of Pathology Search for other works by this author on: Oxford Academic PubMed Google Scholar B. Kaynor, B. Kaynor †Department of Immunopathology Unit Search for other works by this author on: Oxford Academic PubMed Google Scholar C. A. Howard, C. A. Howard †Department of Immunopathology Unit Search for other works by this author on: Oxford Academic PubMed Google Scholar K. M. Bain, K. M. Bain †Department of Immunopathology Unit Search for other works by this author on: Oxford Academic PubMed Google Scholar I. F. Palacios, I. F. Palacios ‡Department of Cardiac Unit, Massachusetts General HospitalBoston, Massachusetts, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. T. Fallon J. T. Fallon *Department of Pathology Address for correspondence: Dr J. T. Fallon, Department of Pathology, Massachusetts General Hospital, Fruit Street, Boston, MA 02114, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar European Heart Journal, Volume 8, Issue suppl_J, November 1987, Pages 195–197, https://doi.org/10.1093/eurheartj/8.suppl_J.195 Published: 01 November 1987
Background: Patent foramen ovale (PFO) is an independent risk factor of ischemic stroke. It enables the mixing of venous and arterial blood and therefore serves as a conduit for venous clots and vasoactive factors to enter into arterial circulation and contribute to a prothrombotic status. Asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of nitric oxide synthase, contributes to vascular disease and has been linked with increased levels of homocysteine, which creates additional oxidative stress by decreasing the production of dimethylarginine dimethlyaminohydrolase (DDAH) and further inhibiting the clearance of ADMA. We previously identified a significant reduction of homocysteine by PFO closure. Here we study the influence of PFO on ADMA levels, a marker of oxidative stress. Method: 97 PFO-related stroke patients were prospectively recruited in accordance with IRB, of which 61 received PFO closure and 36 underwent medical therapy alone. Peripheral venous blood was collected at baseline (BL) and 1 year follow-up (FU) post treatments. Plasma ADMA was quantified by mass spectrometry. Result: Compared to baseline, plasma ADMA levels were statistically significantly reduced post PFO closure (p = 0.0026), while no changes were observed for the patients treated with medications alone (p = 0.5500) (Figure 1A). Moreover, among the patients receiving PFO closure, the reduction of ADMA was only pronounced for those without residual shunting (p = 0.0009) but not for those with residual shunting (p = 0.4557) (Figure 1B, C). Conclusion: PFO closure reduced oxidative stress marker ADMA in the circulation, but no changes were observed in patients on medical treatment only or those with residual shunting post PFO closure. Our results support the hypothesis that PFO-related right-to-left interatrial blood shunting may causally contribute to the high level of vasoactive factors in circulation. Further studies on an expanded cohort of PFO patients are ongoing.
We report the incidence, management and clinical outcome of coronary perforations in 39 of 12,658 patients (0.3%) undergoing percutaneous coronary intervention (PCI). Coronary perforation occurred more frequently with debulking techniques than with non-debulking (percutaneous transluminal coronary angioplasty and stent) techniques (1% versus 0.2%; p<0.001). There were 8 type I (20.5%), 15 type II (38.5%) and 16 type III (41%) perforations. Importantly, fifty-one percent of the coronary perforations were guide-wire related. Major adverse clinical outcomes occurred more frequently in patients who experienced type III perforations. Conventional strategies to treat perforations (i.e., prolonged balloon inflation and reverse of the anticoagulated state) were used. There was one death (2.6%), two emergency surgeries (5.2%) and no Q-wave myocardial infarctions. Pericardial effusion occurred in 18 of 39 patients (46.2%), with cardiac tamponade occurring in 7 patients. In the current device era, the incidence of coronary perforation remains low; it occurs more frequently with debulking devices and is often a consequence of guidewire injury. Its outcome is not affected with the use of IIb/IIIa antagonists. Treatment of coronary perforation requires early detection, angiographic classification, immediate occlusion of coronary vessel extravasation and relief of hemodynamic compromise, reversal of heparin anticoagulation, platelet transfusion in those patients treated with abciximab and cover stents.
