Angiology

There is conflicting evidence regarding the effectiveness of remote ischemic preconditioning (RIPC) in patients undergoing elective percutaneous coronary intervention (PCI). Therefore, we prospectively enrolled elderly patients with coronary heart disease (CHD) with diabetes mellitus (DM) undergoing elective drug-eluting stent (DES) implantation. They were randomized to receive RIPC within 2 hours before PCI (n = 102) or not (controls, n = 98). Baseline clinical characteristics were similar between the 2 groups. Despite a trend toward decline, the median high-sensitivity cardiac troponin I (hscTnI) level (P = .256) and the incidence of myocardial infarction (MI) type 4a (P = .106) in the RIPC group 16 hours after PCI procedure was not significantly different from the control group. The RIPC could attenuate the release of a myocardial biomarker but failed to show a significant effect on hscTnI level or MI type 4a incidence after PCI procedure in elderly patients with CHD having DM undergoing elective DES implantation.

The pathogenesis of acute brain ischemia (ABI) is highly complex and involves multiple mechanisms including free radical generation. Imbalance between the cellular production of free radicals and the ability of cells to defend against them is referred to as oxidative stress. Oxidative stress is one of the mechanisms contributing to neuronal damage, potentially induced through the ABI. Through interactions with a large number of molecules, reactive oxygen species may irreversibly destroy or alter the function of the cellular lipids, proteins, and nucleic acids and initiate cell signaling pathways after cerebral ischemia. Future investigations should focus on the understanding of oxidative stress mechanisms and neuroprotection in order to discover new treatment targets.

We performed an analysis to assess the need for conducting additional randomized controlled trials (RCTs) comparing open and endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA). Trial sequential analysis (TSA) is a statistical methodology that can calculate the required information size of a meta-analysis and assess the risk of random errors similar to interim analysis in a single optimally powered trial. It helps to decide whether we have obtained sufficient evidence or whether further RCTs are required. For short-term mortality reintervention rates, TSA showed firm evidence that there would be no extra benefit in conducting more RCTs to detect the effectiveness of EVAR versus open repair. For long-term mortality, TSA revealed either inconclusive evidence to support or refute endovascular or open repair; so, further RCTs should be performed to investigate long-term, all-cause mortality after AAA repair.

We compared apoptosis, cellular oxidative stress, and inflammation of cultured endothelial cells treated with sera from 130 patients with peripheral artery disease (PAD) and a control group of 36 patients with high burden of comorbid conditions and cardiovascular risk factors. Second, we compared circulating inflammatory, antioxidant capacity, and vascular biomarkers between the groups. The groups were not significantly different (P > .05) on apoptosis, hydrogen peroxide, hydroxyl radical antioxidant capacity, and nuclear factor κ-light-chain enhancer of activated B cells. Circulating tumor necrosis factor α (TNF-α; P = .016) and interleukin 8 (IL-8; P = .006) were higher in the PAD group, whereas vascular endothelial growth factor A (VEGF-A; P = .023) was lower. The PAD does not impair the endothelium beyond that which already occurs from comorbid conditions and cardiovascular risk factors in patients with claudication. However, patients with PAD have lower circulating VEGF-A than the control group and higher circulating inflammatory parameters of TNF-α and IL-8.

The main aim of the present study was to investigate the association between epicardial adipose tissue (EAT) and arterial function in patients with asymptomatic hypertension. Patients with hypertension (n = 155) were enrolled consecutively. Patients with decreased arterial compliance (AC) and increased cardioankle vascular index (CAVI) had higher EAT values compared with those with normal AC and CAVI (6.23 ± 1.67 vs 4.91 ± 1.40, P < .001 and 6.02 ± 1.61 vs 4.96 ± 1.46, P = .01, respectively). Analysis using the receiver–operating characteristics curve demonstrated that EAT 5.5 mm constitutes the cutoff value for the presence of increased CAVI with 67% sensitivity and 62% specificity (area under the curve [AUC]: 0.702, 95% confidence interval [CI] 0.590-0.814) and decreased AC with 77% sensitivity and 65% specificity (AUC: 0.756, 95% CI 0.645-0.867). Assessment of EAT during echocardiography examination may provide information on arterial function in patients with asymptomatic hypertension. The link between EAT and arterial stiffness deserves further investigation.

Our goal was to estimate the role of high-density lipoprotein cholesterol (HDL-C) in predicting the prevalence and extent of coronary artery disease (CAD) in 3280 patients undergoing coronary angiography. Predictors of lower HDL levels (<32 mg/dL) were male gender (P < .001), diabetes mellitus (P = .03), renal failure (P = .01), higher low-density lipoprotein and total cholesterol (P < .001, respectively), triglycerides (P < .001), and white blood cells (P < .001), aging (P < .001), previous myocardial infarction (P = .02) and hemoglobin (P < .001), treatment with angiotensin-receptor blockers (P < .001), and statins (P = .002). The HDL-C levels were significantly inversely associated with prevalence of CAD (P < .001, adjusted odds ratio [OR] [95% confidence interval, CI] = 1.35 [1.25-1.45], P < .001), and HDL-C <44 mg/dL was best the predictive value of the risk of CAD, (adjusted OR [95%CI] = 1.61 [1.24-2.1], P < .001). We found significant association between HDL-C and the risk of CAD; a value <44 mg/dL was the best cutoff in the prediction of CAD.

Data are scarce regarding emergency medical service (EMS) usage by patients with acute coronary syndrome (ACS) in the Arabian Gulf region. This 9-month in-hospital prospective ACS registry was conducted in Arabian Gulf countries, with 30-day and 1-year follow-up mortality rates. Of 5184 patients with ACS, 1293 (25%) arrived at the hospital by EMS. The EMS group (vs non-EMS) was more likely to be male, have cardiac arrest on presentation, be current or exsmokers, and have moderate or severe left ventricular dysfunction and ST-segment elevation myocardial infarction (STEMI). The EMS group had higher crude mortality rates during hospitalization and after hospital discharge but not after adjustment for clinical factors and treatments. The EMSs are underused in the Arabian Gulf region. Short- and long-term mortality rates in patients with ACS are similar between those who used and did not use EMS. Quality improvement in the EMS infrastructure and establishment of integrated STEMI networks are urgently needed.

To identify predictors of the presence of coronary artery disease (CAD) in patients with planned surgery for aortic aneurysms, we reviewed clinical profiles and angiography records of 191 patients with aortic aneurysms (34 thoracic, 137 abdominal, and 20 thoracoabdominal; 162 men; mean age, 75.2 ± 7.7 years). The incidence of CAD was 38.7% among all the patients. Patients with CAD had significantly low levels of high-density lipoprotein cholesterol (HDL-C) as compared with patients without CAD (45 ± 9 vs 51 ± 13 mg/dL; P = .009). Multivariate analysis showed that only low HDL-C levels were associated with the presence of CAD (adjusted odds ratio, 0.946; 95% confidence interval, 0.911-0.983; P = .004). The optimal cutoff level of HDL-C to predict CAD was 47.50 mg/dL. The CAD is common in patients with aortic aneurysms, and low levels of HDL-C are independently associated with the presence of CAD.

We investigated whether children with a previous Kawasaki disease (KD) have evidence of abnormal vascular and/or platelet function. We included 14 patients with previous KD and 14 matched controls. We assessed endothelial function by flow-mediated dilation (FMD), carotid intima–media thickness (cIMT), coronary microvascular function by coronary blood flow response (CBFR) to cold pressor test, and platelet reactivity by measuring monocyte–platelet aggregates (MPAs) and CD41-platelet expression by flow cytometry. No differences were found between the groups in FMD, cIMT, or CBFR to cold pressor test. The MPAs were similar in patients with KD and controls. CD41-platelet expression, however, was significantly increased in patients with KD compared with controls, both at rest (14.3 ± 1.9 vs 12.4 ± 1.9 mean fluorescence intensity [mfi], P = .01) and after adenosine diphosphate stimulation (19.3 ± 1.3 vs 17 ± 1.7 mfi, P < .001). In conclusion, children with a previous episode of KD showed increased platelet activation, compared with healthy participants despite no apparent vascular abnormality at follow-up.

Acute brain ischemia caused by transient ischemic attack initiates a complex sequence of events in the central nervous system and hypothalamic–pituitary–adrenal (HPA) axis which may ultimately culminate in neuronal and cell damage. The brain is highly susceptible to ischemia and in response to stress shows changes in morphology and chemistry that are largely reversible. These responses are known to modify the function of the HPA axis, but their mechanisms are not yet clear. Duration and size of the HPA axis activation are regulated by corticotropin-releasing hormone, vasopressin (AVP), and glucocorticoids, including cortisol. Numerous studies suggest that activation of these hormones following brain ischemia can result in neurohormonal dysfunction that can exacerbate long-term prognosis following stroke. These studies represent evidence that changes in the HPA axis play an important role in brain ischemia.

A low high-density lipoprotein cholesterol (HDL-C) level is a predictor of increased cardiovascular risk. We assessed the mean platelet volume (MPV) in patients with low HDL-C. We studied 59 patients with low HDL-C (HDL-C ≤35 mg/dL) and 56 control participants (HDL-C levels >35 mg/dL) with similar cardiovascular risk factors. As expected, HDL-C was significantly lower among the patients with low HDL-C than that of the control group (32 ± 3 vs 51 ± 5 mg/dL, respectively; P < .001). Platelet count was significantly lower among the patients with low HDL-C than that of the control group (213 ± 60 vs 285 ± 75 × 10⁹/L, respectively; P < .001). The MPV was significantly higher among the patients with low HDL-C than that of the control group (8.7 ± 0.6 vs 7.1 ± 0.5 fL, respectively; P < .001). We have shown that MPV was significantly elevated in patients with low HDL-C compared with control participants.

We investigated 2 hypotheses: (1) a relationship between platelet indices and stable coronary artery disease (CAD) and acute ST-segment elevation myocardial infarction (STEMI) and (2) a relationship between platelet indices on admission and thrombolysis outcomes in patients with STEMI. A total of 260 patients were enrolled. The white blood cell (WBC) and platelet distribution width (PDW) were found to be increased in patients with STEMI (P for both < .001). White blood cell and PDW were independent predictors of acute STEMI. Mean platelet volume (MPV) and PDW were significantly higher in the thrombolysis failure group than in the thrombolysis success group (9.9 ± 1.8 vs 9.2 ± 1.5 fL, P = .021 and 17.7 ± 1.0 vs 16.4 ± 2.1 fL, P < .001, respectively). Mean platelet volume and PDW were independent predictors of thrombolysis failure. Patients with acute STEMI had higher PDW than did patients with stable CAD. In addition, higher PDW and MPV seem to correlate with thrombolysis failure in patients with STEMI.

Nondipper pattern of blood pressure (BP) is associated with cardiovascular risk. In this study, we compared dipper versus nondipper patterns between normotensive patients with panic disorder (PD) and a control group. A total of 25 normotensive patients with PD and 25 controls were enrolled. Twenty-four-hour ambulatory BP monitoring was performed in all patients. At least 10% of sleep-related nocturnal decrease in systolic and diastolic BP was accepted as dipper status, while decreases <10% were defined as a nondipper. Patients with PD had significantly higher incidence of nondipper BP pattern than controls. The reduction of nighttime BP in both systolic and diastolic and mean BP was significantly lower in patients with PD than in the control group (7.6% ± 4.3% vs 13% ± 3.9%, P < .001; 11% ± 7% vs 15% ± 5%, P = .004; 9% ± 5% vs 14% ± 4%, P = .002, respectively). Panic disorder is associated with nondipper BP pattern, causing impaired circadian BP in normotensive settings.