Association between pneumococcal vaccination and cardiovascular outcomes: a systematic review and meta-analysis of cohort studies.

AIMS: Streptococcus pneumoniae is the most common cause of community-acquired pneumonia (CAP) and CAP-related mortality in adults. Pneumococcal vaccination (PV) could protect subjects from cardiovascular events by reducing pneumonia severity or even preventing it. We sought to determine the ability of PV to protect from the risk of cardiovascular events. METHODS AND RESULTS: A comprehensive search of electronic databases was conducted up to March 2014. Cohort studies that reported relative risk (RR) estimates with 95% confidence intervals (CI) were included. Eleven studies were included (332,267 participants, mean follow-up 20.1 months). The pooled RRs for cardiovascular events and cardiovascular mortality were 0.86 (95% CI: 0.76-0.97) and 0.92 (95% CI: 0.86-0.98; fixed-effects), respectively, for subjects with PV versus without PV. Protective ability was more prominent in high cardiovascular risk populations and with older age. The protective role of PV was attenuated after 1 year (RR: 0.72; 95% CI: 0.59-0.88 vs RR: 1.03; 95% CI: 0.93-1.14; p = 0.002, for follow-up >1 year vs ≤1 year, respectively). It also increased as the presence of cardiovascular and pulmonary disease increased. Regarding myocardial infarction (MI) and cerebrovascular events, the protective role of PV was statistically significant only in the elderly (RR: 0.90; 95% CI: 0.817-0.999; fixed-effects and RR: 0.86; 95% CI: 0.75-0.99, respectively). CONCLUSION: PV is associated with decreased risk of cardiovascular events and mortality. This protective effect increases at older age and in high cardiovascular risk subjects and decreases as the time elapses from PV. PV decreases the risk of MI and cerebrovascular events in the elderly.

Prediction of cardiovascular events and all-cause mortality with erectile dysfunction: a systematic review and meta-analysis of cohort studies.

BACKGROUND: Erectile dysfunction (ED) carries an independent risk for cardiovascular (CV) events. We conducted a meta-analysis of all longitudinal studies for determining the ability of ED to predict risk of clinical events and to dissect factors influencing this ability. METHODS AND RESULTS: We conducted a comprehensive search of electronic databases through July 2012. Longitudinal studies that reported relative risk (RR) estimates with 95% confidence intervals (CIs) were included. Of the 14 studies included (92 757 participants; mean follow-up, 6.1 years; 16 articles), 13 (14 articles) reported results on total CV events (91 831 individuals), 4 on CV mortality (34 761 individuals), 4 on myocardial infarction (35 523 individuals), 6 on cerebrovascular events (27 689 individuals), and 5 on all-cause mortality (17 869 individuals). The pooled RRs for the above-mentioned end points were 1.44 (95% CI, 1.27-1.63), 1.19 (95% CI, 0.97-1.46), 1.62 (95% CI, 1.34-1.96), 1.39 (95% CI, 1.23-1.57), and 1.25 (95% CI, 1.12-1.39), respectively, for men with versus without ED. The RR was higher in intermediate- compared with high- or low-CV-risk populations and with younger age. The RR for studies that diagnosed ED with the use of a questionnaire compared with a single question was higher (RR, 1.61; 95% CI, 1.38-1.86 versus RR, 1.27; 95% CI, 1.18-1.37, respectively; P=0.006). CONCLUSIONS: ED is associated with increased risk of CV events and all-cause mortality. RR is higher at younger ages, in intermediate-risk groups, and when a questionnaire is used instead of a single question.

Relation of habitual cocoa consumption to aortic stiffness and wave reflections, and to central hemodynamics in healthy individuals.

The effect of habitual cocoa consumption on arterial stiffness and wave reflection indexes, as well as on peripheral and central blood pressure, was assessed in 198 healthy subjects. In conclusion, higher cocoa intake was an independent determinant of low arterial stiffness and wave reflection indexes and was also independently associated with significantly lower central (aortic) pulse pressure.

Left ventricular (LV) geometry and dipping state are determinants of LV mass reduction with angiotensin-converting enzyme inhibitor antihypertensive treatment.

OBJECTIVES: Left ventricular hypertrophy is a major risk predictor in hypertensive patients and its regression is beneficial in terms of prognosis. The aim of this observational, open-labeled study was to investigate the effect of left ventricular geometry and dipping pattern on left ventricular mass reduction after chronic treatment with angiotensin-converting enzyme inhibitors, in a large population of hypertensive patients. METHODS: We evaluated untreated patients with mild to moderate essential hypertension, before and 6 months after treatment with angiotensin-converting enzyme inhibitor monotherapy or angiotensin-converting enzyme inhibitor-low-dose thiazide combination. Left ventricular mass index, relative wall thickness and geometry pattern were derived from echocardiography. Dipping state was determined with 24-h ambulatory blood pressure monitoring at enrollment. RESULTS: Overall, left ventricular mass index decrease in the 1400 patients (mean age 52.5 years) who completed the study was 12.9% of baseline value (P<0.00001). After adjusting for pretreatment value, left ventricular mass index reduction was similar with all angiotensin-converting enzyme inhibitors used [P= NS (not significant)], but it was higher in nondippers than dippers (14.1 vs. 12.3%, P<0.0001) and in patients with than without baseline left ventricular hypertrophy (14.6 vs. 11.3%, P<0.0001). We observed a stepwise augmentation of left ventricular mass index decrease with worsening left ventricular geometry (P<0.001). In multivariable analysis, impaired left ventricular geometry and blunted nocturnal blood pressure fall before treatment were independent predictors of a high left ventricular mass index reduction after treatment, independent of blood pressure fall, pretreatment left ventricular mass index, and other potential confounders. CONCLUSION: In essential hypertension, left ventricular geometry and dipping state are independent determinants of left ventricular mass reduction with angiotensin-converting enzyme inhibitor treatment. All angiotensin-converting enzyme inhibitors are efficient in decreasing left ventricular mass.

Hypertensive patients with false-positive thallium-201 scintigraphic results in the infero-posterior wall are in high risk for coronary artery disease development.

BACKGROUND: It has been previously postulated that Thallium-201 (Tl201) scintigraphy is characterized by relatively low specificity in hypertensive patients. This study was undertaken to assess any possible influence of false-positive scintigraphic results on the prognosis of hypertensive patients. METHODS: The study group comprised 179 consecutive hypertensive patients (128 men and 51 women), aged 50+/-7 years, who underwent exercise Tl(201) scintigraphy and coronary angiography (patients with normal scintigraphic results underwent coronary angiography due to persistent angina-like symptoms). All patients with normal coronary arteries underwent a second Tl201 scintigraphy within 36+/-6 months. Patients with reversible ischemia in the second scintigraphy underwent also a second coronary angiography. RESULTS: Coronary artery disease (CAD) was detected in 78 (44%) patients, while the rest 101 (56%) patients had normal coronary arteries. Abnormal scintigraphic results were revealed in 66 (85%) patients with CAD and in 38 (38%) patients without CAD. Twenty-two (58%) of the 38 hypertensive patients with false-positive scintigraphic results presented reversible ischemia of the infero-posterior wall of the left ventricle. Coronary artery disease was detected in 7 (32%) of these patients during the follow-up period. CONCLUSIONS: Hypertensive patients with normal coronary arteries and false-positive scintigraphic results usually present with reversible ischemia of the infero-posterior wall of the left ventricle. This group of patients seems to be at increased risk of developing CAD in a long-term follow-up period.

Red wine acutely induces favorable effects on wave reflections and central pressures in coronary artery disease patients.

BACKGROUND: To investigate red wine's acute effects on aortic pressures and arterial stiffness in patients with coronary artery disease (CAD). METHODS: Fifteen patients with CAD were recruited in a double-blind, cross-over study, which was comprised of 2 study days. Each volunteer consumed either 250 mL of regular or 250 mL of dealcoholized red wine. Wave reflections, expressed as augmentation index (AIx), as well as central and peripheral blood pressures (BP) were assessed at fast and 30, 60, and 90 min postprandially. RESULTS: Both regular and dealcoholized red wine caused a significant decrease in AIx by 10.5% +/- 1.4% (P = .001) and 6.1% +/- 1.4% (P = .011), respectively, whereas no significant change was induced in mean BP and timing of wave reflections expressing pulse wave velocity. Peripheral systolic BPs remained unaltered in both beverages, whereas a significant decrease in peripheral and central diastolic BPs was observed after the dealcoholized red wine consumption (P = .03 and P = .035, respectively). Central systolic BP was decreased after the consumption of regular (-7.4 +/- 2.4 mm Hg, P = .05) and dealcoholized red wine (-5.4 +/- 2.7 mm Hg, P = .019). CONCLUSIONS: Both types of red wine provoked favorable acute effects on wave reflections and central systolic pressures, whereas no such effect was evident at the brachial artery. Therefore, these findings could be attributed mainly to red wine antioxidant substances, rendering it a possible means of at least acute attenuation of increased wave reflections, arterial stiffness, and central pressures in patients with coronary artery disease.

Effect of coffee on endothelial function in healthy subjects: the role of caffeine.

Coffee is one of the most widely used pharmacologically active beverages. The present study was designed to evaluate the acute effect of coffee ingestion on endothelial function in healthy individuals, and the potential role of caffeine. We studied 17 healthy young adults (28.9+/-3.0 years old; nine men), who were regular non-heavy coffee drinkers. The endothelial performance was estimated by endothelium-dependent FMD (flow-mediated dilatation) of the brachial artery before and 30, 60, 90 and 120 min after ingestion of a cup of caffeinated coffee (80 mg of caffeine) or the corresponding decaffeinated beverage (< 2 mg of caffeine) in two separate sessions, following a randomized single-blind cross-over design. There was no difference in baseline FMD values between the two sessions [7.78 compared with 7.07% after caffeinated and decaffeinated coffee respectively; P = NS (not significant)]. Caffeinated coffee led to a decline of FMD (7.78, 2.86, 2.12, 4.44 and 4.57% at baseline, 30, 60, 90 and 120 min respectively; P < 0.001). This adverse effect was focused at 30 (P = 0.004) and 60 min (P < 0.001). No significant effect on FMD was found with the decaffeinated coffee session (7.07, 6.24, 5.21, 7.41 and 5.20%; P = NS). The composite effect of the type of coffee consumed over time on FMD was significantly different (P = 0.021). In conclusion, coffee exerts an acute unfavourable effect on the endothelial function in healthy adults, lasting for at least 1 h after intake. This effect might be attributed to caffeine, given that decaffeinated coffee was not associated with any change in the endothelial performance.

Endothelial dysfunction and type of cigarette smoked: the impact of 'light' versus regular cigarette smoking.

Acute cigarette smoking leads to temporary endothelial dysfunction, which is an early event in atherogenesis. Sufficient data concerning the effect of cigarettes with low tar and nicotine yield are lacking. Seventeen healthy individuals (nine women, eight men, aged 27.8 +/- 3.6 years) were subjected to evaluation of endothelial function by means of endothelium-dependent, flow-mediated dilatation (FMD) of the brachial artery, before, immediately after and 30, 60 and 90 min after smoking a regular cigarette (nicotine 0.9 mg, tar 12 mg) orthe corresponding 'light' cigarette (nicotine 0.6 mg, tar 8 mg). The following day, measurements were repeated after smoking the opposite kind of cigarette. Baseline FMD was 6.1 +/- 1.6% and 7.2 +/- 2.0% in the light and regular cigarette groups, respectively (p = NS). The overall effect of the regular cigarette over time on FMD compared with the light cigarette was significantly different (F = 3.039, p = 0.023). FMD was significantly depressed after smoking both types (light: F = 8.192, p < 0.001; regular: F = 16.698, p < 0.001). Immediately after smoking, FMD declined in both groups (light: 3.0 +/- 2.4% and regular: 1.6 +/- 3.2%, p < 0.001 and p < 0.001, respectively), and it remained significantly depressed in the regular cigarette group at 30 min (0.75+/-1.5%, p < 0.001) and 60 min (3.5 +/- 3.1%, p = 0.024), while in the light cigarette group FMD differences were abolished at 30, 60 and 90 min after smoking. In conclusion, acute smoking of both regular and light cigarettes leads to temporary vasomotor dysfunction; its duration is shorter after smoking a 'light' cigarette.

The impact of third-generation beta-blocker antihypertensive treatment on endothelial function and the prothrombotic state: effects of smoking.

BACKGROUND: The significance of beta-blockers in the treatment of cardiovascular diseases is well established. The effect of vasodilating beta-blockers on endothelial function and prothrombotic state has not been investigated. METHODS: The study comprised 550 consecutive patients with uncomplicated essential hypertension. They were treated with celiprolol, carvedilol or nebivolol monotherapy (171, 179, and 200 patients, respectively), achieving comparable blood pressure reduction. Plasma levels of fibrinogen and homocystine and serum levels of plasminogen activator inhibitor-1 (PAI-1) were obtained before and 6 months after initiation of treatment. RESULTS: The three drugs differentiated in regard to homocystine (P <.00001) and fibrinogen level changes (P =.00003), but not (P = NS) in PAI-1 change. In smokers, differentiation was found in all three parameters (P =.0002, P =.001, and P =.006 for fibrinogen, PAI-1, and homocystine, respectively), but in nonsmokers differentiation was found only in homocystine change (P =.00003). In smokers, fibrinogen, PAI-1, and homocystine were reduced more (P =.002, P =.0009, and P <.0001, respectively) than in nonsmokers in the whole study cohort. The effect of nebivolol was more prominent in smokers than nonsmokers in reducing all three parameters (P =.0001,.003, and.003, respectively), whereas in celiprolol and carvedilol-treated groups, differentiation between smokers and nonsmokers was significant (P =.00003 and.01, respectively) only in homocystine level change. CONCLUSIONS: In hypertensive smokers, nebivolol resulted in a significant decrease of plasma PAI-1, fibrinogen and homocystine. Celiprolol also significantly affected these parameters but to a lesser degree, whereas carvedilol had no significant favorable action. In nonsmokers, homocystine was reduced significantly by nebivolol. We conclude that smoking status should be a determinant of antihypertensive treatment choice.