Implementation of a Cardiogenic Shock Team in a Tertiary Academic Centre.

BACKGROUND: Observational studies have shown that the management of patients with cardiogenic shock (CS) by dedicated multidisciplinary teams improve clinical outcomes. Nevertheless, these studies reflect a specific organisational setting with most patients being transfers from referring hospitals, hospitalised in cardiac intensive care units (ICU), or treated with mechanical circulatory support (MCS) devices. The purpose of this study was to document the organisation and outcomes of a CS team offering acute care in all-comer population. METHODS: A CS team was developed in a large academic tertiary institution. The team consisted of emergency care physicians, critical care cardiologists, interventional cardiologists, cardiac surgeons, ICU physicians and heart failure specialists and was supported by predefined operating protocol, dedicated communication platform and regular team meetings. RESULTS: Over 12 months, 70 CS patients (69±13 years old, 67% males) were included. Acute myocardial infarction (AMI-CS) was the most common cause (64%); 31% of the patients presented post-resuscitated cardiac arrest and 56% needed invasive mechanical ventilation (IMV). Coronary angiography was performed in 70% and 53% had percutaneous coronary intervention. MCS was used in 10% and 6% were referred for urgent cardiac surgery. The in-hospital mortality in our centre was 40% with 39% of the patients dying within 24-hours from presentation. 76% of the alive patients were discharged home. CONCLUSIONS: Across an all-comer population, AMI was the most common cause of CS. A significant number of patients presented post cardiac arrest, and the majority required IMV. Mortality was high with a significant number dying within hours of presentation.

Emergency department risk assessment and disposition of acute heart failure patients: existing evidence and ongoing challenges.

Heart failure (HF) is a global public health burden, characterized by frequent emergency department (ED) visits and hospitalizations. Identifying successful strategies to avoid admissions is crucial for the management of acutely decompensated HF, let alone resource utilization. The primary challenge for ED management of patients with acute heart failure (AHF) lies in the identification of those who can be safely discharged home instead of being admitted. This is an elaborate decision, based on limited objective evidence. Thus far, current biomarkers and risk stratification tools have had little impact on ED disposition decision-making. A reliable definition of a low-risk patient profile is warranted in order to accurately identify patients who could be appropriate for early discharge. A brief period of observation can facilitate risk stratification and allow for close monitoring, aggressive treatment, continuous assessment of response to initial therapy and patient education. Lung ultrasound may represent a valid bedside tool to monitor cardiogenic pulmonary oedema and determine the extent of achieved cardiac unloading after treatment in the observation unit setting. Safe discharge mandates multidisciplinary collaboration and thoughtful assessment of socioeconomic and behavioural factors, along with a clear post-discharge plan put forward and a close follow-up in an outpatient setting. Ongoing research to improve ED risk stratification and disposition of AHF patients may mitigate the tremendous public health challenge imposed by the HF epidemic.

The Greek study in the effects of colchicine in COvid-19 complications prevention (GRECCO-19 study): Rationale and study design.

OBJECTIVE: Colchicine has been utilized safely in a variety of cardiovascular clinical conditions. Among its potential mechanisms of action is the non-selective inhibition of NLRP3 inflammasome which is thought to be a major pathophysiologic component in the clinical course of patients with COVID-19. GRECCO-19 will be a prospective, randomized, open-labeled, controlled study to assess the effects of colchicine in COVID-19 complications prevention. METHODS: Patients with laboratory confirmed SARS-CoV-2 infection (under RT PCR) and clinical picture that involves temperature >37.5 oC and at least two out of the: i. sustained coughing, ii. sustained throat pain, iii. Anosmia and/or ageusia, iv. fatigue/tiredness, v. PaO2<95 mmHg will be included. Patients will be randomised (1:1) in colchicine or control group. RESULTS: Trial results will be disseminated through peer-reviewed publications and conference presentations. CONCLUSION: GRECCO-19 trial aims to identify whether colchicine may positively intervene in the clinical course of COVID-19. (ClinicalTrials.gov Identifier: NCT04326790).

Beneficial Effects of Vaccination on Cardiovascular Events: Myocardial Infarction, Stroke, Heart Failure.

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 streptococcus pneumoniae in CHD, HF and stroke and highlights its beneficial effect in the reduction of adverse cardiovascular events.

Cellular Communications in the Heart.

Heart failure is one of the leading causes of morbidity and mortality worldwide. Cardiac remodelling is first an adaptive, becoming a maladaptive, compensatory mechanism that finally causes ventricular dysfunction independently of the etiology of the initial insult. In the present article the authors describe the elements of the human heart, examining their basic functions and their inter-communication under both normal and pathological circumstances. Cardiac myocytes carry out mechanical and electrical functions of the heart and cardiac fibroblasts maintain its structural integrity. Several factors can affect fibroblast activation and under pathological stress they transdifferentiate into myofibroblasts. Endothelial cells have complex biological functions, including the control of vascular permeability, vasomotion, regulation of haemostasis, immune responses and angiogenesis. The extracellular matrix is a complex architectural network consisting of a variety of proteins. Various routes using a plethora of products and mediators contribute to the cross-talk of the myocytes with endothelial cells, extracellular matrix and cardiac fibroblasts. A better understanding of the entire mechanism of cellular communication by the established or the more recently discovered agents will certainly emerge promising new perspectives when looking at the prevention of heart failure and leading to more substantial therapeutic interventions.

Clinical and neurohormonal correlates and prognostic value of serum prolactin levels in patients with chronic heart failure.

AIMS: Hypothalamic axis deregulation is associated with clinical severity and depression in chronic heart failure (CHF). We investigated the relationship of serum prolactin, an indicator of hypothalamic axis function, to neurohomonal/immune activation and depressive symptoms in CHF as well as its prognostic value. METHODS AND RESULTS: Serum prolactin was determined in 180 patients with advanced CHF (aged 65 ± 12 years, mean LVEF 27 ± 7%) along with natriuretic peptides (BNP), inflammatory cytokines, endothelial adhesion molecules, 6 min walk test (6MWT), and the Zung self-rating depression scale (SDS). Patients were followed for all-cause death or hospitalization for cardiovascular reasons for up to 8 months. Prolactin levels were significantly correlated with NYHA class (r = 0.394, P < 0.001), LVEF (r = -0.314, P < 0.001), 6MWT (r = -0.353, P < 0.001), BNP (r = 0.374, P < 0.001), Zung SDS (r = 0.544, P < 0.001), interleukin-6 (IL-6) (r = 0.451, P < 0.001), IL-10 (r = -0.426, P < 0.001), tumour necrosis factor (TNF)-α (r = 0.310, P = 0.001), soluble Fas (r = 0.333, P < 0.001), soluble Fas-ligand (r = 0.517, P < 0.001), soluble intercellular adhesion molecule-1 (ICAM-1) (r = 0.409, P < 0.001), and soluble vascular cell adhesion molecule-1 (VCAM-1) (r = 0.480, P < 0.001). During follow-up, 119 patients (66%) died or were hospitalized for cardiovascular events after a median time of 72 days (range 5-220 days); these patients had higher baseline prolactin levels (10.2 ± 5.7 vs. 6.7 ± 4.3 ng/mL, P < 0.001), and a prolactin value ≥4.5 ng/mL was associated with a higher rate of death or hospitalization (116 ± 7 vs. 181 ± 11 days, P = 0.0001). In multivariate analysis, prolactin levels remained an independent predictor of death or hospitalization (<4.5 vs. ≥4.5 ng/mL; odds ratio, 0.368; 95% confidence interval 0.148-0.913; P = 0.031), along with BNP (P < 0.001) and 6MWT (P = 0.020). CONCLUSIONS: Serum prolactin is associated with neurohormonal/immune activation and depressive symptoms and is an independent predictor of prognosis in advanced CHF.

Arterial stiffness is associated with increased monocyte expression of adiponectin receptor mRNA and protein in patients with coronary artery disease.

BACKGROUND: Arterial stiffness and carotid intima-media thickness (IMT) constitute validated cardiovascular prognostic markers. Adiponectin and its receptors 1 (AdipoR1) and 2 (AdipoR2) are involved in coronary artery disease (CAD). We investigated whether AdipoR1 and R2 mRNA and protein expression are associated with arterial stiffness, IMT and extent of coronary atherosclerosis. METHODS: We studied 71 patients (61 men, 10 women) with angiographically proven CAD. We measured: (i) monocyte expression of AdipoR1 and AdipoR2 mRNA (quantitative real-time PCR) and protein expression (flow cytometry) (iii) adiponectin, metalloproteinase-9 (MMP-9) and C-reactive protein (CRP) blood levels, (iv) carotid-femoral artery pulse wave velocity (PWV) and carotid IMT. RESULTS: Patients with multi-vessel CAD had higher AdipoR1 and AdipoR2 mRNA than those with single-vessel (P < 0.05). PWV was associated with AdipoR1 mRNA (r = 0.474), AdipoR1 protein (r = 0.228), AdipoR2 mRNA (r = 0.716), AdipoR2-protein (r = 0.261), adiponectin (r = 0.236), and MMP-9 (r = 0.350) (P < 0.05, for all correlations). After adjustment for age, sex, waist-hip ratio, and mean blood pressure both AdipoR1 and AdipoR2 mRNA remained independent determinants of PWV (R(2) = 0.35 and R(2) = 0.57, P < 0.05). IMT was also associated with AdipoR2 mRNA, AdipoR2 protein, and MMP-9 (P < 0.05). Increased expression of ADR2 mRNA significantly related to MMP-9 (r = 0.210), and CRP (r = 0.531) (P < 0.05). CONCLUSION: Increased mRNA and protein expression of adiponectin receptors is related with increased aortic stiffness, coronary and peripheral atherosclerosis in patients with CAD. The interrelation of AdipoR2 with inflammatory markers, PWV and IMT suggests a compensatory increase of these receptors to counteract the excess inflammatory and atherogenic process in CAD. Thus, adiponectin receptors may provide a potential therapeutic target of agents activating their beneficial action.American Journal of Hypertension 2012; doi:10.1038/ajh.2012.42.

Managing the underestimated risk of statin-associated myopathy.

In clinical practice 5-10% of patients receiving statins develop myopathy, a side effect that had been systematically underestimated in the randomized controlled trials with statins. The most common manifestation of myopathy is muscle pain (usually symmetrical, involving proximal muscles) without creatinine kinase (CK) elevation or less frequently with mild CK elevation. Clinically significant rhabdomyolysis (muscle symptoms with CK elevation >10 times the upper limit of normal and with creatinine elevation) is extremely rare. Myopathy complicates the use of all statins (class effect) and is dose-dependent. The pathophysiologic mechanism of statin-associated myopathy is unknown and probably multifactorial. The risk of statin-associated myopathy can be minimized by identifying vulnerable patients (i.e. patients with impaired renal or liver function, advanced age, hypothyroidism, etc.) and/or by eliminating-avoiding statin interactions with specific drugs (cytochrome P-450 3A4 inhibitors, gemfibrozil, etc.). In symptomatic patients, the severity of symptoms, the magnitude of CK elevation and the risk/benefit ratio of statin continuation should be considered before statin treatment is discontinued. Potential strategies are the use of the same statin at a lower dose and if symptoms recur the initiation of fluvastatin XL 80 mg daily or rosuvastatin intermittently in low dose (5-10mg), combined usually with ezetimibe 10mg daily. Failure of these approaches necessitates the use of non-statin lipid lowering drugs (ezetimibe, colesevelam). In order to provide evidence based recommendations for the appropriate management of statin-intolerant patients we need randomized clinical trials directly comparing the myopathic potential of different lipid-lowering medications at comparable doses.

Staccato reperfusion improves myocardial microcirculatory function and long-term left ventricular remodelling: a randomised contrast echocardiography study.

OBJECTIVE: 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 (ß) and flow (A×ß) 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 A(n), ß and A×ß at 48 h, 1 and 12 months after intervention compared with AR (mean A×ß: 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 A(n) 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 A(n), ß and A×ß (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.

G-455A polymorphism of beta-fibrinogen gene and the risk of premature myocardial infarction in Greece.

INTRODUCTION: There are limited and controversial data regarding the impact of G-455A polymorphism of beta-fibrinogen gene in the pathogenesis of premature myocardial infarction (MI). We examined whether the G-455A polymorphism of beta-fibrinogen gene is associated with the development of MI< or =35 years of age. METHODS: We recruited 181 consecutive patients who had survived their first acute MI< or =35 years of age (mean age=32.2+/-3.4 years). The control group consisted of 129 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease. G-455A polymorphism of beta-fibrinogen was tested with polymerase chain reaction and reverse hybridization. RESULTS: There was a higher prevalence of carriers of the A allele (GA+AA genotype) in controls than in patients (odds ratio [OR] 0.57, 95% confidence interval [CI] 0.36 to 0.91, p=0.02). G-455A polymorphism of beta-fibrinogen gene was associated with lower risk for acute MI (OR 0.46, 95% CI 0.25 to 0.83, p=0.01) after adjusting for major cardiovascular risk factors. Fibrinogen levels were higher in patients compared to controls [332 (292-385) vs. 311 (262-373) mg/dL, p=0.01], but the adjusted for classical risk factors fibrinogen levels did not differ (OR 1.003, 95% CI 0.99 to 1.01, p=0.37). Patients possessing the A allele did not differ in their fibrinogen and lipid levels compared to patients with the -455GG genotype. CONCLUSIONS: Our data indicate that the presence of the G-455A polymorphism of beta-fibrinogen gene has a "protective effect" against the development of non-fatal acute MI< or =35 years of age in Greece.

Recurrent vasovagal syncope: comparison between clomipramine and nitroglycerin as drug challenges during head-up tilt testing.

AIMS: 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). METHODS AND RESULTS: 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. CONCLUSION: 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.

Long-term nonoutflow septal versus apical right ventricular pacing: relation to left ventricular dyssynchrony.

BACKGROUND: Right ventricular (RV) apical pacing deteriorates left ventricular (LV) function. RV nonoutflow (low) septal pacing may better preserve ventricular performance, but this has not been systematically tested. Our aim was to assess (1) whether long-term RV lower septal pacing is superior to RV apical pacing regarding LV volumes and ejection fraction (EF), and (2) if the changes in LV dyssynchrony imposed by pacing are related to the long-term changes in LV volumes and EF. METHODS: In thirty-six patients with atrioventricular (AV) block, a dual-chamber pacemaker was implanted. The ventricular electrode was placed either at the apex or at the lower septum, in a randomized sequence. Twenty-four to 48 hours following implantation, we measured LV volumes, EF, and LV dyssynchrony (by tissue Doppler imaging), both with and without pacing. Patients were reassessed echocardiographically after 12 months. RESULTS: Lower septal pacing induced a more synchronized pattern of LV contraction changes (P < 0.05). Following 12 months, differences were observed between groups regarding LV volumes and EF. EF increased within the septal group (from 52 +/- 3.3% to 59 +/- 3.0%, P < 0.05). A significant inverse relation was documented between changes in LV dyssynchrony and changes in EF (r =-0.64, P < 0.05). CONCLUSIONS: In patients with AV block, RV nonoutflow septal pacing represents an attractive alternative, since it preserves better and may even improve LV volumes and EF. Late changes in EF are associated with the changes in LV dyssynchrony imposed by pacing.

The predictive value of inflammatory and oxidative markers following the successful cardioversion of persistent lone atrial fibrillation.

BACKGROUND: Although there is evidence that inflammation and oxidative stress might contribute to the pathogenesis of atrial fibrillation (AF), the predictive value of inflammatory and oxidative stress markers in patients with AF has not been fully assessed. The aim of this study is to evaluate these markers as predictors of sinus rhythm (SR) maintenance, in patients with persistent lone AF. METHODS: Among 268 patients with symptomatic AF, we studied 46 patients with a first episode of recently established persistent lone AF. We measured the circulating levels of hs-CRP, TNF-alpha, IL-6, IL-10, sICAM-1, sVCAM-1, malondialdehyde (MDA) and nitrotyrosine (NT) before, 1 h, 24 h, 1, 2, 4 and 6 weeks after cardioversion. During a 12-month follow-up period, AF recurrence was evaluated by Holter ECG recordings every month and when symptoms were reported. RESULTS: Baseline levels of CRP, TNF-alpha, sICAM-1, MDA, and NT were elevated in patients with AF compared to controls, and higher in patients with than in those without persistent AF recurrence, while IL-6 levels were equally elevated in the two subgroups. SR maintenance was associated with lower baseline MDA values and faster decrease in IL-6, sICAM-1 and NT levels within the first 2 weeks following SR restoration. CONCLUSIONS: Increased markers of inflammation and oxidative stress are found in patients with lone AF, implying that inflammation and oxidative stress may be associated with the presence of the arrhythmia. IL-6, sICAM-1, MDA and NT, assessed prior to and after the first cardioverted episode of persistent arrhythmia, appear to be reliable, early predictors of SR maintenance during the following year.

Staccato reperfusion prevents reperfusion injury in patients undergoing coronary angioplasty: a 1-year follow-up pilot study.

BACKGROUND: Adjunctive interventions protect from reperfusion injury during primary percutaneous coronary intervention (PCI), but it is not known whether they are also protective during elective PCI. We sought to assess the efficacy of staccato reperfusion (SR) during PCI. METHODS: Thirty seven patients with recent acute coronary syndrome and target lesions of 85-100% were randomized to SR (n=18), consisting of 6 periods of 10-s balloon inflation/deflation (total time, 120 sec) or abrupt reperfusion (AR, n=19), consisting of a single continuous 120-s balloon inflation; subsequently, all underwent stent implantation. Left ventricular wall motion score was echocardiography determined at baseline, 10 days and 1 year later. The oxidative markers malondialdehyde (MDA) and nitrotyrosine were assessed at baseline, 3 and 18 min after PCI. Patients were also followed for 1 year for major events (death, non-fatal myocardial infarction or revascularization). RESULTS: Wall motion score index (SR: 1.34+/-0.29 (baseline), 1.17+/-0.17 (10-day), 1.08+/-0.12 (1-year); AR: 1.33+/-0.22, 1.27+/-0.20, 1.24+/-0.22, respectively) improved significantly as a result of SR (F=8.951, p=0.002). Similarly, the biomarkers of oxidative injury, MDA (1.74+/-0.49 micromol/L in SR vs. 2.45+/-1.26 micromol/L in AR, p=0.002) and nitrotyrosine (5.23+/-5.58 nmol/L in SR vs. 9.79+/-7.83 nmol/L in AR, p=0.003) measured 18 min after PCI were significantly lower in SR. No major events occurred. CONCLUSIONS: SR can improve long-term wall motion score during PCI, at least partly through the attenuation of a reperfusion-type oxidative injury that also occurs in these patients.

Vasodilation in vasovagal syncope and the effect of water ingestion.

Abnormal (increased, but also decreased) vasodilative responses have been observed in patients with vasovagal syncope (VVS). The objective was to assess reactive vasodilation in supine patients with VVS and its relation to severity of the syndrome. Reactive vasodilation was also assessed after a simple therapeutic intervention (water drinking). Thirty-four patients were studied, all with recurrent VVS and a recent positive head-up tilt test result. Seventeen matched healthy subjects served as controls. Venous occlusion plethysmography was used to assess forearm blood flow (FBF) and forearm vascular resistance resistance (1) at rest and (2) during reactive hyperemia. Clinical severity of the syndrome was related to the intensity and duration of the vasodilative reflex. The same plethysmographic measurements were repeated 60 minutes after drinking 500 ml of water. Before water drinking, no difference was observed between groups in baseline measurements. However, duration of hyperemia was longer in patients (p <0.05) and was related to the duration of the previous positive tilt test (r = -0.69, p <0.05) and total number of each patient's symptomatic vasovagal episodes (r = 0.49, p <0.05). After water ingestion, baseline FBF decreased in patients (p <0.05) and remained stable in controls. In patients, duration of hyperemia decreased to normal values. Hyperemic FBF remained similar between groups. In conclusion, increased reactive vasodilative reflexes were observed in patients with VVS. They seemed to be of significant pathophysiologic significance. Water drinking can normalize them for >or=60 minutes.

Long-term prognostic factors of young patients (

BACKGROUND: There are few and conflicting data regarding the prognostic role of continued smoking in very young survivors of acute myocardial infraction (AMI) after the event. DESIGN: We conducted a prospective study to evaluate the impact of smoking habits on long-term outcome in individuals who sustained AMI at the age of

Simvastatin exerts its anti-inflammatory effect in hypercholesterolaemic patients by decreasing the serum levels of monocyte chemoattractant protein-1.

AIM: To assess the effect of simvastatin on serum levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-6, tumor necrosis factor-alpha, macrophage colony stimulating factor, C-reactive protein and serum amyloid A in hypercholesterolaemic patients without coronary heart disease. METHODS: Sixty consecutive hypercholesterolaemic patients were randomly assigned in a 2:1 process to 40 mg of simvastatin daily (n=40) and to hypolipidaemic only diet (n=20) for 3 months. Blood was taken at baseline and at the end of the study and analysed for lipids and inflammatory markers. RESULTS: From the inflammatory markers only MCP-1 was decreased significantly (217.4+/-48 versus 177+/-75 pg/ml, p<0.001) after treatment with simvastatin and this reduction was independent of lipid changes. CONCLUSION: Simvastatin significantly decreases only MCP-1 levels in hypercholesterolaemic patients suggesting that this molecule is probably a sensitive marker to detect the anti-inflammatory effect of simvastatin in blood.

Sertraline for the treatment of depression in coronary artery disease and heart failure.

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.

Depression in coronary artery disease: novel pathophysiologic mechanisms and therapeutic implications.

Depression is a common comorbid condition in patients with coronary artery disease and a well-documented risk factor for recurrent cardiac events and mortality. The exact mechanisms underlying the interplay between depression and ischemic heart disease remain poorly understood and the same is true for the most effective depression treatment for cardiac patients. This review summarizes current knowledge regarding the prognostic role of depression in patients with coronary artery disease, the pathophysiologic pathways involved, and the effects of antidepressant therapy on cardiovascular disease outcomes. With recent evidence suggesting that selective serotonin reuptake inhibitors may improve survival after myocardial infarction in patients with depression, diagnosis and treatment of this co-morbidity may be essential for the clinical management of coronary artery disease.

Selective serotonin re-uptake inhibitors for the treatment of depression in coronary artery disease and chronic heart failure: evidence for pleiotropic effects.

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.