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Background: The relationship between alcohol consumption and atherosclerosis has not been sufficiently examined among people living with HIV (PLWH). Methods: We analyzed data from PLWH in the Women's Interagency HIV Study (WIHS; n = 1,164) and the Multicenter AIDS Cohort Study (MACS; n = 387) with no history of cardiovascular disease (CVD). Repeated measures of intima‐media thickness of the right common carotid artery (CCA‐IMT) were assessed using B‐mode ultrasound from 2004 to 2013. Current alcohol consumption was collected at time of CCA‐IMT measurement and was categorized according to gender‐specific weekly limits. Group‐based trajectory models categorized participants into past 10‐year consumption patterns (1994 to 2004). Multivariate generalized estimating equations were conducted to assess the association of past and current alcohol use patterns on change in CCA‐IMT by cohort, controlling for age, race, cigarette and illicit drug use, probable depression, HIV RNA viral load, antiretroviral therapy exposure, and hepatitis C coinfection. Results: Among the WIHS, past heavy alcohol consumption was associated with increased CCA‐IMT level over time (β = 8.08, CI 0.35, 15.8, p = 0.04), compared to abstinence. Among the MACS, compared to abstinence, all past consumption patterns were associated with increased CCA‐IMT over time (past low: β = 15.3, 95% CI 6.46, 24.2, p < 0.001; past moderate: β = 14.3, CI 1.36, 27.2, p = 0.03; past heavy: β = 21.8, CI 4.63, 38.9, p = 0.01). Current heavy consumption was associated with decreased CCA‐IMT among the WIHS (β = −11.4, 95% CI −20.2, −2.63, p = 0.01) and MACS (β = −15.4, 95% CI −30.7, −0.13, p = 0.04). No statistically significant time by consumption pattern effects were found. Conclusions: In both cohorts, 10‐year heavy consumption was associated with statistically significant increases in carotid artery thickness, compared to abstinence. Long‐term patterns of drinking at any level above abstinence were particularly significant for increases in IMT among men, with heavy consumption presenting with the greatest increase. Our results suggest a potentially different window of risk among past and current heavy drinkers. Further studies are needed to determine whether alcohol consumption level is associated with intermediate measures of atherosclerosis. Alcohol screening and interventions to reduce heavy consumption may benefit PLWH who are at risk of CVD. The relationship between alcohol consumption and atherosclerosis has not been sufficiently examined among people living with HIV (PLWH). We analyzed data from PLWH with no history of cardiovascular disease (CVD) using repeated measures of intima‐media thickness and alcohol consumption. Our results suggest a potentially different window of risk among past and current heavy drinkers. Alcohol screening and interventions to reduce heavy consumption may benefit PLWH who are at risk for CVD. [ABSTRACT FROM AUTHOR]

Background: An acute psychological stress can precipitate ventricular arrhythmias and sudden cardiac death in patients with coronary artery disease (CAD). However, the physiologic mechanisms by which these effects occur are not entirely clear. Mental stress-induced myocardial ischemia occurs in a significant percentage of the CAD population. It is unknown if the proarrhythmic effects of psychological stress are mediated through the development of myocardial ischemia. Objectives: To examine the effects of psychological stress on QT dispersion (QTd) among CAD patients and whether these effects are mediated via the development of myocardial ischemia. Methods: Psychological stress was induced using a public speaking task. Twelve-lead electrocardiograms (ECG) were recorded at rest, during mental stress, and during recovery. QTd was calculated as the difference between the longest and the shortest QT interval in the 12-lead ECG. Rest-stress myocardial perfusion imaging was also performed to detect mental stress-induced myocardial ischemia. Results: Mental stress induced a significant increase in QTd compared to the resting condition (P < 0.001). This effect persisted beyond the first 10 minutes of recovery (P < 0.001). QTd was significantly associated with the development of mental stress ischemia with ischemic patients having significantly higher QTd during mental stress than nonischemic patients (P = 0.006). This finding remained significant after controlling for possible confounding factors (P = 0.01). Conclusion: An acute psychological stress induces a significant increase in QTd, which persists for more than 10 minutes after the cessation of the stressor. This effect seems to be, at least partially, mediated by the development of mental stress-induced myocardial ischemia. [ABSTRACT FROM AUTHOR]

This article discusses the link between depression and coronary heart disease (CHD). Particular focus is given to the prevalence of depression in patients CHD, along with the use of the Patient Health Questionnaire in identifyng depressed patients. There is a need for cardiologists to consider depression in the management of CHD. Some of the treatment options for these patients include antidepressant drugs, cognitive behavioral therapy and physical activity.

Abstract: Background: It has been suggested that oxidative stress may play a role in the pathogenesis of heart failure, this may have potential implications for therapeutic strategies. However, measures of oxidative stress are subject to confounding inaccuracies. IgG antibodies to oxidized LDL reflect exposure to the lipoprotein over an extended period and may thus mirror oxidative stress over a prolonged time frame. Therefore, we tested the hypothesis that anti-oxLDL antibodies correlate with the control of heart failure (HF), as manifested by hospital admissions for cardiac dysfunction. Methods: One hundred and two consecutive patients attending the HF clinic with either systolic or diastolic HF were enrolled and the quality of clinical control was evaluated by assessing hospital admissions over the year prior to index determination of the oxidative stress marker. Antibodies to oxLDL were determined by ELISA and pro-BNP levels were also measured. Results: Most patients (mean age 71.5 years) had systolic HF; mean NYHA functional class was 2.7 and mean left ventricular ejection fraction was 39.7%. Anti-oxLDL antibodies, but not pro-BNP, correlated significantly with mean NYHA score (averaged from all clinic visits in the year prior to blood testing), and with hospital admissions over the year prior to blood testing. Mean IgG anti-oxLDL antibody levels in patients with hospital admissions were 3.4 times higher than those in subjects not hospitalized over the previous year. Conclusion: IgG anti-oxLDL antibody levels correlate with the severity of HF. [Copyright &y& Elsevier]

About one third to one half of patients with heart failure are anemic, in that they have a hemoglobin level of less than 12 g/dL. Anemia is more common and more severe as the clinical status of CHF worsens. In addition, anemia is associated with a higher mortality and higher rate of hospitalization, as well as with signs of malnutrition. In anemic CHF patients who are resistant to maximally tolerated CHF medications and who remain very symptomatic, both uncontrolled studies of a combination of subcutaneous erythropoietin (EPO) and IV ferric sucrose have reported a correction of the anemia. This correction has been associated with an improvement in NYHA functional status, left ventricular ejection fraction, and a marked reduction in the doses of diuretic needed and in the frequency and duration of hospitalizations. Renal function, which had been steadily falling before the correction of the anemia, was also stabilized. Other controlled studies have also found that anemia correction with EPO increased oxygen utilization during maximal exercise, exercise endurance and quality to life. The anemia is probably due mainly to a combination of renal failure and excessive cytokines, both of which interfere with EPO production and utilization. If confirmed by larger studies, correction of anemia with the EPO-IV iron combination may become a useful adjuvant to the treatment of CHF. [Copyright &y& Elsevier]

It is widely accepted that patients presenting with acute anterior myocardial infarction and acute onset of right bundle branch block should be prophylactically paced in contrast with those who have a chronic bundle branch block. The admitting physician is faced with the dilemma of how to act if the age of this conduction disturbance is unknown. This problem has further intensified in recent years, with the introduction of thrombolytic treatment, where insertion of a central vascular line is associated with increased morbidity. The objectives of this study were to define clinical or electrocardiographic parameters that may help the admitting physician to decide whether patients presenting with an anterior wall myocardial infarction and a right bundle branch block of unknown age should be prophylactically paced. We examined prospectively the in-hospital clinical course of 39 consecutive patients presenting with an acute myocardial infarction in whom the age of a right bundle branch block upon admission was unknown (group C, n = 39) and compared it with two similar groups of patients who presented with an acute right bundle branch block (group A, n = 38) and with a known chronic right bundle branch block (group B, n = 22). Thirty-three patients (33%) died, with cardiogenic shock being the leading cause of death in the entire population. Prophylactic pacing, which was carried out in 66% and 54% of patients in groups A and C, respectively, did not reduce mortality rates. No clinical or electrocardiographic variables on admission were predictive to support prophylactic pacing in group C. In 10 of 46 (22%) patients who were prophylactically paced with a transvenous electrode, the following complications attributed to the procedure were detected: (1) either rapid sustained ventricular tachycardia (during implantation) that was unresponsive to overdrive pacing, or ventricular fibrillation necessitating electrical defibrillation (4 patients); (2) recurrent episodes of rapid nonsustained ventricular tachycardia, which stopped only after the pacemaker was turned off (1 patient); (3) complete AV block (1 patient); (4) fever appearing on the third or fourth day after implantation (3 patients); and (4) a large hematoma in the groin in 1 patient who was treated with thrombolysis shortly before pacemaker electrode insertion. Thus, the complications of transvenous temporary pacing in the era of thrombolysis may outweigh any theoretical advantage. [ABSTRACT FROM AUTHOR]

As recently described by Moe et al., parasystolic modulation implies that the ectopic cycle length of a parasystolic focus can be increased or decreased by electrical influences transmitted across the zone of protection. A search for this phenomenon was made in nine patients with intermittent ventricular parasystole resulting from protection only during specific portions of the cycle. All nine patients had a period of relatively early protection affecting the initial 55-67% of the cycle preceding a period of resetting during which the parasystolic focus was discharged and fully recycled. In addition, two patients had a period of relatively late parasystolic protection. Pseudo-resetting (apparent resetting in the surface leads without interruption of activity within the parasystolic focus itself), seen throughout the entire period of late protection in these two patients, and during the relatively refractory period in one patient, was identified because the R waves causing apparent resetting were encompassed by parsystolic-to-parasystolic intervals equalling twice the ectopic cycle length. Our findings indicate that parasystolic modulation did not occur in the type of intermittent ventricular parasystole included in this study. That is, the parusystolic focus was either not affected (not modulated) during specific (early or late) portions of the cycle, or normally reset (discharged and fully recycled, but neither depressed, nor enhanced) in other portions of the cycle. This study does not exclude the occurrence of modulation in other types of parasystole, nor in some automatic nonparasystolic rhythms. [ABSTRACT FROM AUTHOR]

BackgroundThe response of progenitor cells (PCs) to transient myocardial ischemia in patients with coronary artery disease remains unknown. We aimed to investigate the PC response to exercise-induced myocardial ischemia (ExMI) and compare it to flow mismatch during pharmacological stress testing. Methods and ResultsA total of 356 patients with stable coronary artery disease underwent 99mTc-sestamibi myocardial perfusion imaging during exercise (69%) or pharmacological stress (31%). CD34 + and CD34 + /chemokine (C-X-C motif) receptor 4 PCs were enumerated by flow cytometry. Change in PC count was compared between patients with and without myocardial ischemia using linear regression models. Vascular endothelial growth factor and stromal-derived factor-1α were quantified. Mean age was 63±9 years; 76% were men. The incidence of ExMI was 31% and 41% during exercise and pharmacological stress testing, respectively. Patients with ExMI had a significant decrease in CD34 + /chemokine (C-X-C motif) receptor 4 (-18%, P =0.01) after stress that was inversely correlated with the magnitude of ischemia ( r =-0.19, P =0.003). In contrast, patients without ExMI had an increase in CD34 + /chemokine (C-X-C motif) receptor 4 (14.7%, P =0.02), and those undergoing pharmacological stress had no change. Plasma vascular endothelial growth factor levels increased (15%, P <0.001) in all patients undergoing exercise stress testing regardless of ischemia. However, the change in stromal-derived factor-1α level correlated inversely with the change in PC counts in those with ExMI ( P =0.03), suggesting a greater decrease in PCs in those with a greater change in stromal-derived factor-1α level with exercise. ConclusionsExMI is associated with a significant decrease in circulating levels of CD34 + /chemokine (C-X-C motif) receptor 4 PCs, likely attributable, at least in part, to stromal-derived factor-1α-mediated homing of PCs to the ischemic myocardium. The physiologic consequences of this uptake of PCs and their therapeutic implications need further investigation.

Background: Mental stress-induced myocardial ischemia (MSIMI) is associated with adverse prognosis in patients with coronary artery disease (CAD), yet the mechanisms underlying this phenomenon remain unclear. We hypothesized that compared with exercise/pharmacological stress-induced myocardial ischemia (PSIMI) that is secondary to the atherosclerotic burden of CAD, MSIMI is primarily due to vasomotor changes., Methods and Results: Patients with angiographically documented CAD underwent 99mTc-sestamibi myocardial perfusion imaging at rest and following both mental and physical stress testing, performed on separate days. The severity and extent of CAD were quantified using the Gensini and Sullivan scores. Peripheral arterial tonometry (Itamar Inc) was used to assess the digital microvascular tone during mental stress as a ratio of pulse wave amplitude during speech compared with baseline. Measurements were made in a discovery sample (n = 225) and verified in a replication sample (n = 159). In the pooled (n = 384) sample, CAD severity and extent scores were not significantly different between those with and without MSIMI, whereas they were greater in those with compared with those without PSIMI (P < 0.04 for all). The peripheral arterial tonometry ratio was lower in those with compared with those without MSIMI (0.55 ± 0.36 versus 0.76 ± 0.52, P = 0.009). In a multivariable analysis, the peripheral arterial tonometry ratio was the only independent predictor of MSIMI (P = 0.009), whereas angiographic severity and extent of CAD independently predicted PSIMI., Conclusions: The degree of digital microvascular constriction, and not the angiographic burden of CAD, is associated with MSIMI. Varying causes of MSIMI compared with PSIMI may require different therapeutic interventions that require further study.