Management of Depression in Patients with Comorbid Cardiovascular Disease

2001 ◽  
Vol 14 (6) ◽  
pp. 526-539
Author(s):  
Leigh Anne Nelson ◽  
Joy R. Abu-Shanab
Keyword(s):  
Cardiovascular Disease ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Platelet Reactivity ◽  
Cardiac Risk ◽  
Cardiac Risk Factor ◽  
Cardiac Morbidity ◽  
Cardiac Side Effects ◽  
Appropriate Treatment ◽  
Increased Risk ◽  
Ventricular Instability

Evidence suggests that depression commonly occurs in patients with cardiovascular disease and is associated with a poor prognosis including increased risk of cardiac mortality. Proposed pathophysiologic mechanisms include decreased heart rate variability, altered sympathetic and parasympathetic activity, increased ventricular instability, and abnormal platelet reactivity. Other proposed mechanisms involve the interference of depression with medication adherence and cardiac risk factor reduction. Despite this evidence, depression during cardiovascular disease is commonly unrecognized and inadequately treated. Tricyclic antidepressants (TCA) are efficacious for treating depression in this population but cause serious cardiac side effects and should be avoided in patients with significant cardiovascular disease. More recent studies with bupropion and the selective serotonin reuptake inhibitors (fluoxetine, paroxetine, sertraline) indicate that they are acceptable alternatives to TCAs with regard to cardiac risk in depressed patients with heart disease, although larger studies are needed to validate their safety and efficacy in this special population. There are 3 studies currently being conducted to investigate the effect of antidepressant therapy and/or psychotherapy on cardiac morbidity and mortality in post–myocardial infarction patients with depression and/or low social support. These studies will hopefully answer the long-posed question of whether appropriate treatment of depression can improve cardiac prognosis.

scholarly journals MicroRNA as Biomarkers for Platelet Function and Maturity in Patients with Cardiovascular Disease

2021 ◽  
Author(s):  
Oliver Buchhave Pedersen ◽  
Erik Lerkevang Grove ◽  
Steen Dalby Kristensen ◽  
Peter H. Nissen ◽  
Anne-Mette Hvas
Keyword(s):  
Cardiovascular Disease ◽  
Platelet Function ◽  
Assessment Tool ◽  
Platelet Reactivity ◽  
Thrombus Formation ◽  
Quality Assessment Tool ◽  
Treatment And Prevention ◽  
Increased Risk ◽  
Meta Analyses ◽  
Potential Use

AbstractPatients with cardiovascular disease (CVD) are at increased risk of suffering myocardial infarction. Platelets are key players in thrombus formation and, therefore, antiplatelet therapy is crucial in the treatment and prevention of CVD. MicroRNAs (miRs) may hold the potential as biomarkers for platelet function and maturity. This systematic review was conducted using the guidelines of Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). To identify studies investigating the association between miRs and platelet function and maturity in patients with CVD, PubMed and Embase were searched on October 13 and December 13, 2020 without time boundaries. Risk of bias was evaluated using a standardized quality assessment tool. Of the 16 included studies, 6 studies were rated “good” and 10 studies were rated “fair.” In total, 45 miRs correlated significantly with platelet function or maturity (rho ranging from –0.68 to 0.38, all p < 0.05) or differed significantly between patients with high platelet reactivity and patients with low platelet reactivity (p-values ranging from 0.0001 to 0.05). Only four miRs were investigated in more than two studies, namely miR-223, miR-126, miR-21 and miR-150. Only one study reported on the association between miRs and platelet maturity. In conclusion, a total of 45 miRs were associated with platelet function or maturity in patients with CVD, with miR-223 and miR-126 being the most frequently investigated. However, the majority of the miRs were only investigated in one study. More data are needed on the potential use of miRs as biomarkers for platelet function and maturity in CVD patients.

scholarly journals The Relationship between Body Mass Index and the Severity of Coronary Artery Disease in Patients Referred for Coronary Angiography

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Anne B. Gregory ◽  
Kendra K. Lester ◽  
Deborah M. Gregory ◽  
Laurie K. Twells ◽  
William K. Midodzi ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Body Mass Index ◽  
Coronary Artery ◽  
Body Mass ◽  
Cardiac Risk ◽  
Cardiac Risk Factor ◽  
Increased Risk ◽  
Specific Mortality ◽  
Artery Disease ◽  
The Relationship

Background and Aim. Obesity is associated with an increased risk of cardiovascular disease and may be associated with more severe coronary artery disease (CAD); however, the relationship between body mass index [BMI (kg/m2)] and CAD severity is uncertain and debatable. The aim of this study was to examine the relationship between BMI and angiographic severity of CAD. Methods. Duke Jeopardy Score (DJS), a prognostic tool predictive of 1-year mortality in CAD, was assigned to angiographic data of patients ≥18 years of age (N=8,079). Patients were grouped into 3 BMI categories: normal (18.5–24.9 kg/m2), overweight (25.0–29.9 kg/m2), and obese (≥30 kg/m2); and multivariable adjusted hazard ratios for 1-year all-cause and cardiac-specific mortality were calculated. Results. Cardiac risk factor prevalence (e.g., diabetes, hypertension, and hyperlipidemia) significantly increased with increasing BMI. Unadjusted all-cause and cardiac-specific 1-year mortality tended to rise with incremental increases in DJS, with the exception of DJS 6 (p<0.001). After adjusting for potential confounders, no significant association of BMI and all-cause (HR 0.70, 95% CI .48–1.02) or cardiac-specific (HR 1.11, 95% CI .64–1.92) mortality was found. Conclusions. This study failed to detect an association of BMI with 1-year all-cause or cardiac-specific mortality after adjustment for potential confounding variables.

Cardiac Morbidity and Mortality after Surgery for Gastrointestinal Carcinomas

2005 ◽  
Vol 71 (10) ◽  
pp. 833-836
Author(s):  
Matthew Lin ◽  
Jason Haukoos ◽  
Amir Tahernia ◽  
Christian De Virgilio
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Cardiac Event ◽  
Event Rate ◽  
Cardiac Risk ◽  
Clinical Risk Factors ◽  
Cardiac Events ◽  
Cardiac Morbidity ◽  
Clinical Risk ◽  
Cardiac Event Rate

The number of Americans undergoing surgery for gastrointestinal (GI) cancer is increasing, as is the prevalence of cardiovascular disease. Clinical risk factors have been found to be useful in predicting cardiac events after vascular procedures. Their utility for predicting cardiac events after GI carcinoma surgery is unclear. We performed a retrospective review in order to determine whether clinical risk factors are useful in predicting cardiac events in patients undergoing GI carcinoma surgery and to ascertain the incidence of postoperative cardiac events. From 1998 to 2003, 333 patients were identified, with an average age of 56 years. One hundred one (30.3%) patients had one or more clinical risk factors. The overall cardiac event rate was 3.9 per cent. Age >70 years was the only risk factor associated with a cardiac event. There was a trend toward increased cardiac risk with increasing number of risk factors. In the absence of clinical risk factors, cardiac events after surgery for GI carcinoma are low. There is an increased cardiac risk in patients >70 years and a trend toward increased cardiac events as the number of clinical risk factors increases.

Cardiovascular disease in systemic lupus erythematosus

2021 ◽  
Vol 2 (3) ◽  
pp. 157-172
Author(s):  
Maureen McMahon ◽  
Richard Seto ◽  
Brian J. Skaggs
Keyword(s):  
Risk Factors ◽  
Systemic Lupus Erythematosus ◽  
Cardiovascular Disease ◽  
Lupus Erythematosus ◽  
Cardiovascular Events ◽  
Subclinical Atherosclerosis ◽  
Cardiac Risk ◽  
Systemic Lupus ◽  
Cardiac Risk Factors ◽  
Increased Risk

Abstract There is a well-known increased risk for cardiovascular disease that contributes to morbidity and mortality in systemic lupus erythematosus (SLE). Major adverse cardiovascular events and subclinical atherosclerosis are both increased in this patient population. While traditional cardiac risk factors do contribute to the increased risk that is seen, lupus disease-related factors, medications, and genetic factors also impact the overall risk. SLE-specific inflammation, including oxidized lipids, cytokines, and altered immune cell subtypes all are likely to play a role in the pathogenesis of atherosclerotic plaques. Research is ongoing to identify biomarkers that can help clinicians to predict which SLE patients are at the greatest risk for cardiovascular disease (CVD). While SLE-specific treatment regimens for the prevention of cardiovascular events have not been identified, current strategies include minimization of traditional cardiac risk factors and lowering of overall lupus disease activity.

Abstract 3477: Platelet Hyper-responsiveness in Aspirin-Treated Patients with Clinical Cardiovascular Disease Compared to Matched High Risk Controls

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Nauder Faraday ◽  
Lisa R Yanek ◽  
Taryn F Moy ◽  
Dhananjay Vaidya ◽  
J. E Herrera-Galeano ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
High Risk ◽  
Platelet Function ◽  
Ex Vivo ◽  
Platelet Reactivity ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Increased Risk

Background: Platelet hyper-responsiveness to activating stimuli during aspirin (ASA) therapy may discriminate between high risk subjects who have developed acute thrombotic cardiovascular disease (CVD) events (coronary disease and stroke) and those who are at increased risk but are disease free. We hypothesized that subjects with documented CVD would have greater platelet reactivity on ASA therapy compared to matched high risk non-CVD subjects. Methods: Subjects (N=228; 61 +/− 8 yrs, 69% male, 60% white) were selected from families with known CVD; 114 had prevalent CVD and were matched on age, sex, and race to 114 apparently healthy controls with risk factors but without clinical CVD. CVD risk factors were measured and therapy adherence was determined by questionnaires. Platelet reactivity on 81 mg ASA/day was determined by whole blood (WB) aggregometry, platelet function analyzer (PFA) closure time, thromboxane B2 (TxB2) release ex vivo , and urinary excretion of 11-dehyrothromboxane B2 (Tx-M) in vivo . Results. CVD cases had greater platelet reactivity by all measures, both unadjusted, and adjusted for age, sex, race and adherence (Table ). Multivariable adjustment for cardiac risk factors and statin therapy eliminated case-control differences for Tx-M, but not for the ex vivo measures of platelet activation. ASA therapy duration in CVD subjects (8.8 +/− 6.2 yrs) was not related to platelet function. Conclusions: Greater residual platelet reactivity exists during ASA therapy in CVD subjects compared to matched high risk controls, even controlling for CVD risk factors and adherence to therapy. The data suggest that platelet hyper-responsiveness during ASA chemoprophylaxis may differentiate patients with CVD from those who are at risk for CVD, but have not developed it. Platelet hyper-responsiveness may be an intrinsic property of CVD, related to as yet unidentified environmental or genetic factors.

Metformin reduces hyper-reactivity of platelets from patients with polycystic ovary syndrome by improving mitochondrial integrity

2015 ◽  
Vol 114 (09) ◽  
pp. 569-578 ◽  
Author(s):  
Amro Elgheznawy ◽  
Rüdiger Popp ◽  
Paul Rogowski ◽  
Imke Dornauf ◽  
Stefan Dröse ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Platelet Reactivity ◽  
Anion Channel ◽  
Metformin Treatment ◽  
Voltage Dependent Anion Channel ◽  
Ovary Syndrome ◽  
Mitochondrial Integrity ◽  
Increased Risk

SummaryPolycystic ovary syndrome (PCOS) is associated with decreased fertility, insulin resistance and an increased risk of developing cardiovascular disease. Treating PCOS patients with metformin improves fertility and decreases cardiovascular complications. Given that platelet activation contributes to both infertility and cardiovascular disease development, we assessed platelet reactivity in PCOS patients and the consequences of metformin treatment. Compared to washed platelets from healthy donors, platelets from PCOS patients demonstrated enhanced reactivity and impaired activation of the AMP-activated kinase (AMPK). PCOS platelets also demonstrated enhanced expression of mitochondrial proteins such as the cytochrome c reductase, ATP synthase and the voltage-dependent anion channel-1. However, mitochondrial function was impaired as demonstrated by a decreased respiration rate. In parallel, the phosphorylation of dynamin-related protein-1 (Drp-1) on Ser616 was increased while that on Ser637 decreased. The latter changes were accompanied by decreased mitochondrial size. In insulin-resistant PCOS patients (HOMA-IR> 2) metformin treatment (1.7 g per day for 4 weeks to 6 months) improved insulin sensitivity, restored mitochondrial integrity and function and normalised platelet aggregation. Treatment was without effect in PCOS patients with HOMA-IR< 2. Moreover, treatment of megakaryocytes with metformin enhanced mitochondrial content and in the same cells metformin enhanced the phosphorylation of the Drp-1 on Ser637 via an AMPK[uni03B1]1-dependent mechanism. In conclusion, the improvement of mitochondrial integrity and platelet reactivity may contribute to the beneficial effects of metformin on cardiovascular disease.

scholarly journals 2042 CYP2C19*2 and PON1 Q192R polymorphisms are associated with platelet reactivity to clopidogrel in Puerto Rican Hispanics with cardiovascular disease

2018 ◽  
Vol 2 (S1) ◽  
pp. 8-8
Author(s):  
Dagmar F. H. Suarez ◽  
Mariana R. Botton ◽  
Stuart A. Scott ◽  
Matthew I. Tomey ◽  
Kyle Melin ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cardiovascular Disease ◽  
Puerto Rican ◽  
Ex Vivo ◽  
Platelet Reactivity ◽  
Antiplatelet Agents ◽  
Group I ◽  
Increased Risk ◽  
History Of ◽  
Artery Disease

OBJECTIVES/SPECIFIC AIMS: High on-treatment platelet reactivity (HTPR) with clopidogrel imparts an increased risk for ischemic events in adults with coronary artery disease. Although more potent antiplatelet agents are available, clopidogrel remains the most commonly used P2Y12 inhibitor in Puerto Rico. Platelet reactivity varies with ethnicity and is influenced by both clinical and genetic variables; however, no clopidogrel pharmacogenetic studies with Puerto Rican patients have been reported. Therefore, we sought to identify clinical and genetic determinants of on-treatment platelet reactivity in a cohort of Puerto Rican patients with cardiovascular disease. METHODS/STUDY POPULATION: We performed a retrospective study of 111 Puerto Rican patients on 75 mg/day maintenance dose of clopidogrel. Patients were allocated into 2 groups: Group I, without HTPR; and Group II, with HTPR. Clinical data was obtained from the medical record. Platelet function was measured ex vivo using the VerifyNow® P2Y12 assay and HTPR was defined as P2Y12 reaction units (PRU)≥230. Genotyping of CYP2C19, ABCB1, PON1, PY2R12, B4GALT2, CES1, and PEAR1 was performed using Taqman® Genotyping Assays. RESULTS/ANTICIPATED RESULTS: The mean PRU across the cohort was 203±61 PRU (range, 8–324), and 42 (38%) patients had HTPR. One in four individuals carried at least 1 copy of the CYP2C19*2 variant allele. Hematocrit and PON1 p.Q192R variant were inversely correlated with platelet reactivity (p<0.05). Multiple logistic regression showed that 27% of the total variation in PRU was explained by a history of diabetes mellitus, hematocrit, CYP2C19*2, and PON1 p.Q192R. Body mass index (OR=1.15; CI: 1.03–1.27), diabetes mellitus (OR=3.46; CI: 1.05–11.43), hematocrit (OR=0.75; CI: 0.65–0.87), and CYP2C19*2 (OR=4.44; CI: 1.21–16.20) were the only independent predictors of HTPR. DISCUSSION/SIGNIFICANCE OF IMPACT: In a representative sample of Puerto Rican patients with cardiovascular disease, diabetes mellitus, hematocrit, CYP2C19*2, and PON1 p.Q192R were associated with on-treatment platelet reactivity. These factors may identify a subset of patients at higher risk for adverse events on clopidogrel in the Hispanic population.

scholarly journals Epigenetic Regulation of F2RL3 Associates with Myocardial Infarction and Platelet Function

2022 ◽  
Author(s):  
Laura Jayne Corbin ◽  
Stephen J White ◽  
Amy Taylor ◽  
Christopher Michael Williams ◽  
Kurt Taylor ◽  
...  
Keyword(s):  
Gene Expression ◽  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Dna Methylation ◽  
Platelet Reactivity ◽  
Atherosclerotic Cardiovascular Disease ◽  
Dna Hypomethylation ◽  
Exon 2 ◽  
Increased Risk

Background: DNA hypomethylation at the F2RL3 locus has been associated with both smoking and atherosclerotic cardiovascular disease; whether these smoking-related associations form a pathway to disease is unknown. F2RL3 encodes protease-activated receptor 4, a potent thrombin receptor expressed on platelets. Given the role of thrombin in platelet activation and the role of thrombus formation in myocardial infarction, alterations to this biological pathway could be important for ischemic cardiovascular disease. Methods: We conducted multiple independent experiments to assess whether DNA hypomethylation at F2RL3 in response to smoking is associated with risk of myocardial infarction via changes to platelet reactivity. Using cohort data (N=3,205), we explored the relationship between smoking, DNA hypomethylation at F2RL3 and myocardial infarction. We compared platelet reactivity in individuals with low versus high DNA methylation at F2RL3 (N=41). We used an in vitro model to explore the biological response of F2RL3 to cigarette smoke extract (CSE). Finally, a series of reporter constructs were used to investigate how differential methylation could impact F2RL3 gene expression. Results: Observationally, DNA methylation at F2RL3 mediated an estimated 34% of the smoking effect on increased risk of myocardial infarction. An association between methylation group (low/high) and platelet reactivity was observed in response to PAR4 stimulation. In cells, CSE exposure was associated with a 4.9 to 9.3% reduction in DNA methylation at F2RL3 and a corresponding 1.7 (95% CI: 1.2, 2.4, p=0.04) fold increase in F2RL3 mRNA. Results from reporter assays suggest the exon 2 region of F2RL3 may help control gene expression. Conclusions: Smoking-induced epigenetic DNA hypomethylation at F2RL3 appears to increase PAR4 expression with potential downstream consequences for platelet reactivity. Combined evidence here not only identifies F2RL3 DNA methylation as a possible contributory pathway from smoking to cardiovascular disease risk, but from any feature potentially influencing F2RL3 regulation in a similar manner.

New Developments in Diagnosis and Therapy of Depression in Cardiovascular Disease

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
F. Lederbogen
Keyword(s):  
Cardiovascular Disease ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Placebo Treatment ◽  
Cardiac Risk ◽  
Recurrent Depression ◽  
Diagnosis And Therapy ◽  
Cardiovascular Prognosis ◽  
Treatment Of Depression ◽  
Patients With Heart Failure ◽  
Depressive Syndromes

Introduction:Repeatedly, it has been demonstrated that depression increases the risk of developing cardiovascular disorders; vice versa, in subjects with pre-existing heart disease, comorbid depression was found to predict an unfavourable cardiovascular prognosis. However, several studies failed to observe that treatment of depression positively influences cardiac risk. Therefore, focus of research has shifted to identification of subjects, who would benefit from antidepressant therapy that is tailored to their individual needs.Method:Search of literature databases, focusing latest goals and advances in diagnosis and therapy of depression in subjects with cardiovascular disease.Results and discussion:Screening cardiac patients for depression seems to result in a different population of depressed patients, as compared with most trials testing antidepressant agents. This different inclusion process obviously favoured oversampling of subjects with minor or reversible depressive syndromes such as adjustment disorders. It is known that in these conditions placebo treatment is powerful, sometimes equalling verum condition in effectiveness.This hypothesis is supported by re-analysis of former studies revealing selective serotonin reuptake inhibitors (SSRI) to be more effective in subjects with severe or recurrent depression or in patients, in whom depression had begun prior to the onset of cardiovascular disease (e.g., myocardial infarction). Surprisingly, some data support the notion that treatment with SSRIs ameliorates cardiac prognosis irrespective of their antidepressant action. Ongoing studies deal with treatment of depression in patients with heart failure or stroke, and with psychotherapy aimed at reducing cardiac risk factors.

Cardiac arrhythmias related to psychiatric medication

2017 ◽  
Vol 36 (09) ◽  
pp. 747-750
Author(s):  
R. W. Freudenmann ◽  
C. Schönfeldt-Lecuona ◽  
B. J. Connemann ◽  
M. Gahr ◽  
M. Elsayed
Keyword(s):  
Cardiac Arrhythmias ◽  
Torsade De Pointes ◽  
General Medicine ◽  
Fold Increase ◽  
Cardiac Risk ◽  
Psychiatric Medication ◽  
Cardiac Side Effects ◽  
Torsade De Pointes Tachycardia ◽  
Multiple Drugs ◽  
Available Information

SummaryThis narrative review summarizes current available information about cardiac arrhythmias (QT prolongation, Torsade de pointes Tachycardia [TdP], sudden cardiac death) associated with psychiatric medication. Among the most commonly used antipsychotics, amisulpride and ziprasidone are most frequently associated with TdP. Treatment with some antidepressants (SSRIs, tricyclic antidepressants) is associated with a 5- to 6-fold increase in the incidence of out-of-hospital cardiac arrest. Lithium is associated with bradycardia, T-wave changes and AV-block; anxiolytics of the benzodiazepine group do usually not have cardiac side effects. The combination of multiple drugs (including medications from general medicine) that prolong the QT interval has a particularly high cardiac risk.

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