To investigate the effects of staccato reperfusion (SR) during percutaneous coronary intervention (PCI) on myocardial microcirculatory function as assessed by myocardial contrast echocardiography.
Setting
Tertiary centre.
Methods
Thirty-nine patients were randomised to SR (n=20) or abrupt reperfusion (AR, n=19) within 48 h of an acute coronary syndrome. Contrast intensity replenishment curves were constructed to assess the blood volume (An), velocity (β) and flow (A×β) of the segments associated with the PCI-treated artery before, 48 h, 1 and 12 months after PCI. Left ventricular (LV) end-diastolic (EDVs) and systolic volumes (ESVs) were evaluated. Plasma malondialdehyde (MDA) was determined immediately before and 18 min after PCI to assess oxidative stress.
Results
SR was related to a greater improvement in An, β and A×β at 48 h, 1 and 12 months after intervention compared with AR (mean A×β: 0.91, 5.5, 7.14, 6.9 for SR vs 1.02, 3.34, 4.28, 3.71 for AR, p<0.01). After PCI, the mean MDA change was −27% in SR patients and +55% in the AR patients (p<0.05). The percentage change in MDA correlated with the percentage change in An at all time points (r=0.468, r=0.682, r=0.674, p<0.01). Compared with AR, SR was related to a greater percentage decrease in EDV (−11.61% vs −4.13%) and ESV (−34.68% vs −14.83%) at 12 months after PCI (p<0.05). The percentage change in ESV at 12 months correlated with the corresponding percentage changes in An, β and A×β (r=−0.410, r=−0.509, r=−0.577, respectively, p<0.05).
Conclusions
SR improves myocardial microcirculatory function after PCI, leading to a concomitant improvement in LV geometry, probably through reduction of oxidative stress.
Adiponectin, an adipose tissue secreted protein, exhibits anti-inflammatory and antiatherogenic properties. We examined the effects of the globular and full-length adiponectin on cytokine production in macrophages derived from Coronary Artery Disease (CAD) patients and control individuals. Adiponectin's effects in human macrophages upon lipopolysaccharide (LPS) treatment were also examined. Full length adiponectin acted differently on TNF-α and IL-6 production by upregulating TNF-α and IL-6 protein production, but not their mRNA expression. Additionally, full length adiponectin was unable to abrogate LPS proinflammatory effect in TNF-α and IL-6 mRNA expression in CAD and NON-CAD macrophages. In contrast, globular adiponectin appeared to have proinflammatory properties by potently upregulating TNF-α and IL-6 mRNA and protein secretion in human macrophages while subsequently rendered cells resistant to further proinflammatory stimuli. Moreover, both forms of adiponectin powerfully suppressed scavenger MSR-AI mRNA expression and augmented IL-10 protein release, both occurring independently of the presence of LPS or CAD. These data indicate that adiponectin could potentially protect human macrophages via the elevated IL-10 secretion and the suppression of MSR-AI expression. It can also be protective in CAD patients since the reduced adiponectin-induced IL-6 release in CAD macrophages compared to controls, could be beneficial in the development of inflammation related atherosclerosis.
Objectives: Little is known about the impact of body mass index (BMI) on implementation of life saving therapies in patients hospitalized with acute heart failure (AHF) before admission and after stabilization. The present analysis was conducted to explore the relationship of BMI with drug prescription before hospitalization and at discharge in AHF patients. Methods: ALARM-HF is an observational survey on hospitalized patients with AHF in 9 countries (6 European, Turkey, Mexico and Australia). The diagnosis and classification of AHF were based on the ESC guidelines. This subanalysis assesses differences in drug utilization on admission and at discharge in 3,924 AHF patients categorized by BMI in three groups: A <24.9 kg/m2, B 25-29.9 kg/m2 (normal/mild overweight) and C ≥30 kg/m2 (obese). Results: Most patients (65%) had a BMI > 25 kg/m2 (38% in group B and 27% obese). There was no difference in baseline left ventricular ejection fraction among groups. Patients in group B presented more frequently with systolic blood pressure >121 mmHg (A 16.7% vs B 21.8% vs C 16.9%, p <0.001) and were more likely to be treated with diuretics (A 9.2% vs B 11.3% vs C10.1%, p <0.001), ACEi (A 9.9% vs B 12.4% vs C 9.8%, p = 0.002), ARBs (A 7.3% vs B 10.3% vs C 8.9%, p < 0.001), beta-blockers (A 6.8% vs B 9.7% vs C 6.8%, p = 0.001), oral/TTS nitrates (A 2.3% vs B 3.5% vs C 2.6%, p =0.012), and digoxin (A 3.4% vs B 3.9% vs C 3.6%, p = 0.024) on admission. Similarly at discharge, patients in group B patients were more likely to receive diuretics (A 20.6% vs B 26.6% vs C 19.7%, p <0.001), ACEi (A 19.5% vs B 24.0% vs C 17.5%, p = 0.002), ARBs (A 13.8% vs B 19.7% vs C 15.2%, p<0.001), beta-blockers (A 10.4% vs B 14.4% vs C 11.2%, p <0.001), oral/TTS nitrates (A 6.4% vs B 8.6% vs C 6.1%, p =0.046) and tended to receive digoxin more frequently (A 7.3% vs B 8.2% vs C 6.8%, p = 0.082). Use of calcium channel blockers did not differ among the various BMI groups both on admission and at discharge. Patients of group A well as obese patients (group C) had the greatest rate for all-cause in-hospital mortality whereas patients of group B had the lowest rate of adverse outcome (A 9.9% vs B 7.6% vs C 9.8%, p = 0.049). Conclusion: In AHF patients, BMI affects the prescription of chronic medications before admission and at discharge. Normal/ mild overweight patients have been treated more frequently with disease-modifying drugs, such as ACEi/ARBs and beta-blockers, which may be related with the favorable in-hospital outcome.
Background:The aim of this study was to compare the effects of nebivolol and telmisartan on left ventricular mass (LVM) and midwall mechanics in mild-to-moderate hypertension.
Objectives: Observational data suggest that there is a potentially protective effect of increased body mass index (BMI) in chronic heart failure (HF) with reduced left ventricular ejection fraction...
To compare the responses between clomipramine, a centrally acting substance, and nitroglycerin, with mainly peripheral action, when each drug is used during tilt test for the induction of vasovagal syncope (VVS).Hundred patients with recurrent episodes of classical VVS underwent two tilt tests in a randomized sequence. One test included 20 min of tilt at 60 degrees with intravenous administration of 5 mg clomipramine (clomipramine tilt), whereas the other test included an initial 30 min period of passive 60 degrees tilt, followed by sublingual spray administration of 400 microg nitroglycerin (nitroglycerin tilt). Fifty asymptomatic subjects served as controls. Following clomipramine tilt, a positive response occurred in 73 patients (73%), a negative response in 23 (23%), and drug intolerance in 4 (4%). With nitroglycerin tilt, these percentages were 52, 48, and 0%, respectively. Significant differences were observed regarding positive responses (clomipramine vs. nitroglycerin: 73/100 vs. 52/100, P < 0.05), as well as negative responses (23/100 vs. 48/100, respectively, P < 0.05). A high concordance rate was observed in positive responses.In the evaluation of patients with recurrent classical VVS, clomipramine tilt is associated with an increased positive yield relative to nitroglycerin tilt. This suggests that central mechanisms may be more important than peripheral ones in VVS pathogenesis.
Influenza and pneumococcal infections have been suggested to be potential risk factors for causing adverse cardiovascular events, especially in high-risk patients. Vaccination against respiratory infections in patients with established cardiovascular disease (CVD) could serve as a potential cost-effective intervention to improve their clinical outcomes and cardiac societies have encouraged it. Previous studies have shown that influenza vaccination reduce mortality, acute coronary syndromes and hospitalization in patients with coronary heart disease (CHD) and/or heart failure (HF). However, there is a paucity of randomized prospective clinical trials in the field of the pneumococcal vaccination, and additional higher-quality evidence is needed. Furthermore, questions around the role of vaccination in the primary prevention of CVD, the optimal dose and timing are largely unanswered. The pathophysiologic mechanism in which vaccination provides cardiovascular protection may be related to the modification of the immune-inflammatory model of atherogenesis. The present review summarizes the current evidence and understanding for vaccination against influenza and <i>streptococcus pneumoniae</i> in CHD, HF and stroke and highlights its beneficial effect in the reduction of adverse cardiovascular events.
Depression is a common co-morbidity in patients with cardiovascular diseases such as chronic coronary artery disease, acute coronary syndromes, post by-pass surgery and chronic heart failure. There is a significant body of evidence suggesting that the presence of depression is independently associated with a decline in health status and an increase in the risk of hospitalization and death for patients with coronary artery disease or congestive heart failure. Novel treatment modalities such as selective serotonin re-uptake inhibitors (SSRIs) may improve depressive symptoms and prognosis of post-myocardial infarction and heart failure patients interacting with the common pathophysiologic mechanisms of depression and cardiovascular disease. This review summarizes current experimental and clinical evidence regarding the pleiotropic effects of SSRIs on platelet functions, immune and neurohormonal activation, and cardiac rhythm disturbances in patients with cardiovascular disease. These bio-modulatory properties of SSRIs may be translated into improvement of patient clinical outcomes beyond their anti-depressant action. Keywords: SSRIs, depression, cardiovascular disease, platelets, cytokines
Depression is a common co-morbid condition in patients with cardiac disease and has been identified as an independent risk factor for increased morbidity and mortality. SSRIs are established agents for the treatment of depression and are well tolerated in patients with cardiac disease. SSRIs are a heterogeneous group of antidepressants, which apart from their common mechanism of action, differ substantially in their chemical structure, metabolism and pharmacokinetics. This article reviews experimental and clinical evidence on the safety and efficacy of the most extensively studied SSRI, sertraline, in depressed patients with coronary artery disease and heart failure. Intervention with sertraline has the potential to provide depressed patients with cardiac disease relief from their depressive symptoms, improvement in quality of life and a potential benefit in their cardiovascular risk profile.
