Intramural dyssynchrony and response to cardiac resynchronization therapy in patients with and without previous right ventricular pacing.

AIMS: Right ventricular (RV) pacing is an iatrogenic cause of heart failure (HF) that has not been well studied. We assessed whether HF patients paced from the right ventricle (RVp) adversely remodel and respond to cardiac resynchronization therapy (CRT) in a similar way to HF patients without right ventricular pacing (nRVp). METHODS AND RESULTS: Echocardiograms were performed before and ∼5 months after CRT in 31 RVp and 49 nRVp HF patients. Longitudinal intraventricular dyssynchrony using tissue Doppler imaging (TDI) was calculated as the standard deviation of time to peak systolic displacement by tissue tracking (SD-TT) of 12 segments. Longitudinal dyssynchrony within a wall (intramural dyssynchrony) was assessed by two methods: quantifying the number of segments with initial abnormal apical displacement (IMD score) and using a cross-correlation synchrony index (CCSI). Despite similar ejection fractions (EFs) of 28% prior to CRT, left ventricular end-diastolic volume was significantly smaller (143±54 vs. 183±62, P=0.004) in RVp. The standard deviation of time to peak systolic displacement by tissue tracking (83.4±34.9 vs. 67.9±26.6, P=0.03) and IMD score (3.1±1.8 vs. 1.3±1.7, P<0.001) were greater in RVp. Cardiac resynchronization therapy significantly improved EF and volumes in both groups. Ejection fraction increased more in RVp (12.8±9.2% vs. 7.4±7.6%, P=0.007). Intraventricular dyssynchrony and both measures of intramural septal dyssynchrony improved to a greater extent post-CRT in RVp. CONCLUSION: Right ventricular pacing patients differ from nRVp HF patients in that they have smaller ventricles and greater intraventricular and intramural septal dyssynchrony. Right ventricular pacing HF patients respond better to CRT with greater improvements in EF, and intraventricular and intramural septal dyssynchrony.

Intramural dyssynchrony from acute right ventricular apical pacing in human subjects with normal left ventricular function.

Ventricular pacing causes early myocardial shortening at the pacing site and pre-stretch at the opposing ventricular wall. This contraction pattern is energetically inefficient and may lead to decreased cardiac function. This study was designed to describe the acute effects of right ventricular apical (RV(a)) pacing on dyssynchrony and systolic function in human subjects with normal left ventricular (LV) function and compare these effects to pacing from alternate ventricular sites. Patients (n = 26) undergoing an electrophysiology evaluation were studied during atrial pacing (AAI) and dual chamber pacing from the RV(a), left ventricular free wall (LV(fw)), and the combination of RV(a) and LV(fw) (BiV). Tissue Doppler imaging was used to measure intramural dyssynchrony by utilizing an integrated cross-correlation synchrony index (CCSI) from the apical 4-chamber view. RV(a) and BiV pacing significantly reduced systolic function as measured by longitudinal systolic contraction amplitude (SCA(long)) (p < 0.05) and LV velocity time integral (VTI) (p < 0.05) compared to AAI and LV(fw) pacing. RV(a) (and to a lesser extent BiV) pacing resulted in septal and lateral intramural dyssynchrony as indicated by significantly (p < 0.05) lower CCSI values as compared to AAI. CCSI was significantly (p < 0.05) worse during RV(a) than LV(fw) pacing. In patients with normal LV function, acute ventricular pacing in the RV(a) alone, or in conjunction with LV(fw) pacing (BiV), results in impaired regional and global LV systolic function and intramural dyssynchrony as compared to LV(fw) pacing alone.

Multi-plane mechanical dyssynchrony in cardiac resynchronization therapy.

BACKGROUND: The aims of this study were to assess the ability of several echo measures of dyssynchrony to predict CRT response and to characterize the global effect of CRT. HYPOTHESIS: We hypothesized that after CRT there would be significant reductions in mechanical dyssynchrony in all 3 orthogonal planes of cardiac motion and that those patients with significant dyssynchrony prior to implant would have the best echocardiographic response. METHODS: Standard echocardiograms were performed pre-CRT and post-CRT (138 +/- 63d) in 70 heart failure patients. Longitudinal dyssynchrony was calculated as the standard deviation (SD) of time to peak systolic displacement and velocity of 12 segments from 3 apical views. Using midventricular short axis views and speckle-tracking methods, the SD of time to peak radial and circumferential strain in 6 segments were calculated. Cardiac resynchronization therapy echo response was defined as > or = 15% decrease in left ventricular end-systolic volume. RESULTS: Cardiac resynchronization therapy significantly improved systolic function in the longitudinal, radial, and circumferential planes. The CRT echo response rate was 57%. Echo responders (CRT(R)) had significantly (P < .05) more dyssynchrony at baseline as compared to nonresponders (CRT(NR)). Cardiac resynchronization therapy significantly (P < .05) reduced longitudinal and radial, but not circumferential, dyssynchrony in CRT(R). Dyssynchrony was unchanged in CRT(NR). Receiver-operator characteristic (ROC) curve analysis indicated significant, but modest sensitivity and specificity for longitudinal and radial intraventricular dyssynchrony and for interventricular dyssynchrony. Combining radial and longitudinal dyssynchrony measures improved positive prediction of CRT response. CONCLUSIONS: Cardiac resynchronization therapy improves left ventricular function in 3 orthogonal planes of motion. Longitudinal, radial, and interventricular dyssynchrony modestly predict reverse remodeling.

Global electrophysiological and hemodynamic assessment of ventricular pacing employing non-contact mapping.

OBJECTIVE: Right ventricular (RV) pacing has been associated with abnormal cardiac electrical and mechanical dyssynchrony, resulting in impaired global and regional ventricular pump function. This study aimed to characterize the relative effects of pacing site on left ventricular (LV) activation patterns and associated hemodynamic performances. METHODS: Acute pacing was performed in anesthetized swine (n=10) instrumented for RV and LV pressure, noncontact mapping (NCM) of endocardial unipolar electrograms, surface ECG, aortic flow, and sonomicrometry. Bipolar endocardial pacing leads were positioned in the right atrial appendage (RAA), RV apex (RVA), and RV outflow tract (RVOT), while bipolar epicardial leads were positioned on the LV-free wall (LVFW) and LV apex (LVA). RESULTS: LVFW and RVA pacing induced the largest increase in intraventricular electrical dyssynchrony (IVED; 32.2+/-10 ms, 21.7+/-4.1 ms, respectively; both p<0.01), whereas pacing from all sites increased QRS and total endocardial LV activation durations (p<0.01). The largest impairment of LV and RV contractility (dP/dtmax) and relaxation (dP/dtmin) was observed during RVA pacing (p= ns). Synchronous electrical activation patterns were observed on NCM during RVOT and LVA pacing. LVFW pacing was the only site that significantly increased tau values as compared to RAA pacing (approximately 25%), whereas LVA pacing elicited only slight increases (approximately 1%). CONCLUSIONS: In swine with preserved ventricular conduction, in vivo pacing of the RVOT and LVA was associated with preserved, physiologically similar electrical activation sequences and LV function relative to RAA pacing. In contrast, RVA pacing caused widespread electrical dyssynchrony of the LV and prolonged activation durations, thereby impairing associated cardiac performance. Such insights into alternate site cardiac pacing, which employed the combination of high-resolution electrical mapping with real-time hemodynamic assessments, may further increase acute and long-term benefits in patients requiring permanent pacemaker support.

Diet revision in overweight children: effect on autonomic and vascular function.

In an effort to determine the effect of a 5-month dietary modification on measures of vascular and cardiac autonomic (cANS) function in overweight (OW) children, 15 OW children had standard non-invasive measures of vascular and cANS function assessed pre- and post intervention. Body fat percentage and cANS, but not vascular, function changed significantly after the intervention. Changes in body composition in OW children due to dietary modification alone can result in modest improvements in indices of cardiac risk.

Rosiglitazone improves endothelial function and inflammation but not asymmetric dimethylarginine or oxidative stress in patients with type 2 diabetes mellitus.

We compared the vascular effects of rosiglitazone versus glyburide and evaluated asymmetric dimethylarginine (ADMA) and oxidative stress as potential mechanisms associated with changes in vascular health in patients with type 2 diabetes mellitus (T2DM). Patients were randomized to 6 months of either rosiglitazone (n = 20) or glyburide (n = 16) in addition to metformin. The following variables were measured pre- and post-treatment: glucose, insulin, homeostasis model assessment (HOMA), hemoglobin A1c (HbA1c), C-peptide, blood pressure, lipids, C-reactive protein (CRP), ADMA, 8-isoprostane, oxidized LDL cholesterol, brachial artery flow-mediated dilation (FMD), endothelium-independent dilation (EID), and brachial and carotid artery stiffness. Rosiglitazone and glyburide treatment resulted in significant and equivalent decreases in glucose (p < 0.0001) and HbA1c (p < 0.0001), with a trend toward decreased HOMA (p = 0.09). Rosiglitazone significantly decreased C-peptide (p < 0.01) with a strong trend toward decreased fasting insulin (p = 0.05). Rosiglitazone reduced CRP compared with glyburide (p = 0.001), but no differences were observed between groups for ADMA or the markers of oxidative stress. Rosiglitazone significantly improved FMD (p < 0.05) with trends toward improvements in carotid artery distension (p = 0.099) and distensibility (p = 0.078). In conclusion, compared with glyburide, rosiglitazone improves endothelial function and CRP in patients with T2DM. These improvements are not associated with reductions in ADMA or markers of oxidative stress.

Effects of carvedilol versus metoprolol on endothelial function and oxidative stress in patients with type 2 diabetes mellitus.

BACKGROUND: Data suggest that carvedilol possesses antioxidant properties that might provide vascular protection. We sought to compare the effects of carvedilol and metoprolol tartrate on endothelial function and oxidative stress in a head-to-head trial. METHODS: Thirty-four patients with type 2 diabetes mellitus (T2DM) and hypertension were randomized to receive either carvedilol (n = 16) or metoprolol (n = 18) in addition to their current antihypertensive medications for 5 months. The following variables were measured pre- and posttreatment: blood pressure, fasting glucose and insulin, insulin resistance by homeostasis-model assessment, hemoglobin A1c, lipids, C-reactive protein (CRP), 8-isoprostane, asymmetric dimethylarginine, oxidized LDL cholesterol, ultrasound assessment of brachial-artery flow-mediated dilation (FMD), nitroglycerin-induced endothelium-independent dilation (EID), brachial and carotid artery distension, distensibility and compliance, and carotid artery intima-media thickness (cIMT). RESULTS: Both carvedilol and metoprolol treatment resulted in significant and similar decreases in systolic (P < .05) and diastolic (P < .0001) blood pressure. Compared with metoprolol, carvedilol significantly improved FMD (P < .001). No differences between groups were noted for any of the glycemic or lipid variables except for HDL cholesterol, which significantly decreased (P < .05) in the metoprolol group compared with the carvedilol group. No differences were observed between groups for CRP, the markers of oxidative stress, EID, arterial stiffness, or cIMT. CONCLUSIONS: Compared with metoprolol, carvedilol significantly improves endothelial function in patients with T2DM. Changes in glycemic control and oxidative stress do not seem to explain the observed improvements in FMD, which suggests that other mechanisms may be involved.

Relationships of cardiac autonomic function with metabolic abnormalities in childhood obesity.

OBJECTIVE: The objective was to examine cardiovascular autonomic (cANS) function and its potential relationships with leptin resistance, insulin resistance, oxidative stress, and inflammation in a pediatric sample with varying levels of obesity. RESEARCH METHODS AND PROCEDURES: Participants were normal-weight (NW; BMI <85th percentile, 6 male, 4 female), overweight (OW; 85th percentile < BMI <95th percentile, 6 male, 4 female), and obese children (OB; BMI >95th percentile, 6 male, 10 female) who had cANS function assessed via heart rate variability (HRV) methods during resting conditions. Standard time-domain and frequency-domain measures [high-frequency normalized units (HFnu; measure of parasympathetic nervous system activity) and low frequency:high-frequency ratio (LF:HF; overall sympathovagal balance)] of HRV were calculated. Fasting blood samples were drawn for measurement of glucose, insulin, lipids, 8-isoprostane, leptin, soluble leptin-receptor (sOB-R), C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha). Results were reported as mean +/- standard error of the mean. RESULTS: OB had significantly elevated LF:HF and decreased HFnu when compared with NW (p < 0.05), but no differences between OW and NW were observed. Measures of HRV were significantly related to leptin, insulin resistance, 8-isoprostane, and CRP (p < 0.05), but these relationships were not significant after adjustment for fat mass. DISCUSSION: When compared with NW, OB but not OW children are characterized by cANS dysfunction and increased leptin, insulin resistance, oxidative stress, and inflammation (CRP). The relationships between these factors seem to be dependent on quantity of fat mass and/or other factors associated with being obese.

Relationships between heart rate variability, vascular function, and adiposity in children.

OBJECTIVE: To examine the relationships and interactions between cardiovascular autonomic nervous system (cANS) function, adiposity, and vascular function in children of varying levels of adiposity. METHODS: Participants were children (19 M, 17 F, age = 11.5 +/- 0.1 years) who had cANS function assessed via heart rate variability (HRV) methods during resting conditions. Vascular function was assessed with brachial artery flow-mediated dilation (FMD) and nitroglycerin-induced dilation. Spectral power of HRV was calculated for high frequency normalized units (HFnu; measure of PSNS activity) and low frequency:high frequency ratio (LF:HF; overall sympathovagal balance). A blood sample was drawn for measurement of fasting insulin, glucose, lipids, and C-reactive protein (CRP). Results were reported as mean +/- SEM. RESULTS: FMD peak dilation was positively related to HFnu (r = 0.48, P = 0.01) and negatively related to LF:HF (r = -0.51, P = 0.01) indicating that reduced parasympathetic activity and states of dysfunctional sympathovagal balance were associated with decreased vascular function. After adjustment for confounding factors (insulin, CRP, age) and fat mass, the relationships between these measures of cANS and vascular function remained moderately strong and significant. DISCUSSION: These data indicate a relationship between cANS and vascular function that is independent of fat mass, inflammation (CRP), and fasting insulin in children of varying levels of adiposity. These relationships and the mechanisms by which they exist require further study to allow for the identification of appropriate therapies for children with high levels of adiposity given the likelihood of them having concomitant cANS and vascular dysfunction.

Role of nitric oxide deficiency and its detection as a risk factor in pre-hypertension.

Systemic inhibition of nitric oxide (NO) synthesis raises blood pressure, and endothelial dysfunction with reduced NO bioactivity is a precursor of atherosclerosis. Pre-hypertensive blood pressures place patients at increased risk for cardiovascular morbid events. Whether NO deficiency contributes to this increased risk has not been explored. Constitutive NO release was inhibited by infusion of the substituted arginine NG-nitro-L-arginine-methyl ester (L-NAME) in 10 normal volunteers. Hemodynamics, radial artery pulse contour analysis, brachial artery ultrasound, and aortic pulse wave velocity were monitored as well as plasma neurohormone levels. A modest rise in blood pressure within the normotensive range (113/65 to 124/77 mm Hg, P < .01) was accompanied by a rise in estimated systemic vascular resistance (1193 to 1514 dyne-sec-cm-5, P < .001). Pulse contour analysis revealed a fall to abnormal levels in systemic small artery elasticity (diastolic decay) (9.8 to 6.4 ml/mm Hg, P < .001) and a less consistent but significant increase in the second pressure peak in systole (P < .05). Large artery elasticity index, brachial artery caliber, and brachial artery compliance were unchanged. Flow-mediated brachial artery dilation was blunted slightly (5.29% to 4.47%, P = .06), and aortic pulse wave velocity increased slightly but significantly (8.25 to 8.98 m/s, P = .04), probably as a result of the rise in pressure. The magnitude of effect of L-NAME on small artery elasticity (-31.2% +/- 18.4%) was significantly greater and more consistent than its effect on other vascular measurements. Circulating neurohormonal vasoconstrictor levels fell or were unchanged after L-NAME, and a significant reduction in plasma norepinephrine was closely inversely correlated with the rise in blood pressure. Nitroglycerin infusion in 4 additional subjects produced selective relaxation in small arteries, whereas norepinephrine constricted both small and large arteries. A hemodynamic state consistent with pre-hypertension was induced by NO synthase inhibition in normal volunteers. Reduction in small artery compliance was a sensitive marker for this induced endothelial dysfunction and may serve as a useful marker for pre-hypertensive patients at risk for cardiovascular morbid events.

Effects of weight loss on insulin sensitivity and arterial stiffness in overweight adults.

Obesity is characterized by metabolic and vascular abnormalities. We examined the effects of weight loss on insulin sensitivity and arterial stiffness in overweight adults. Twelve (9 females; 3 males) overweight (body mass index, 30.3 +/- 3.7) adults (54.9 +/- 3.9 years) without diabetes or vascular disease were counseled by a registered dietician to lose weight over 6 months. Vascular structure, function, and wall mechanical properties were measured via ultrasound. Intravenous glucose tolerance test, 24-hour blood pressure, body composition (dual-energy x-ray absorptiometry), and lipids were also assessed. There were significant reductions in body mass (86.3 +/- 14.2 vs 79.5 +/- 13.8 kg, P < .0001) and percentage of fat (44.3% +/- 7.0% vs 41.0% +/- 8.5%, P < .01) after weight loss. There were significant improvements in total cholesterol (6.0 +/- 0.9 vs 5.0 +/- 0.8 mmol/L, P < .0001), low-density lipoprotein cholesterol (3.9 +/- 0.7 vs 3.2 +/- 0.6 mmol/L, P < .0001), triglycerides (3.4 +/- 2.3 vs 2.4 +/- 0.9 mmol/L, P < .05), and insulin sensitivity (3.3 +/- 1.7 vs 5.4 +/- 1.6 microU x 10(-4) min(-1) mL(-1), P < .0001) after weight loss. Brachial artery compliance (P < .05) and distensibility (P < .05) curves over the physiologic pressure range improved, whereas endothelial function and intima-media thickness remained unchanged. In overweight adults, 6 months of weight loss resulted in improvements in body composition, insulin sensitivity, lipid profile, and brachial artery compliance and distensibility.

The effects of quinapril and atorvastatin on the responsiveness to sildenafil in men with erectile dysfunction.

Phosphodiesterase-5 (PDE-5) inhibitors are an effective therapy for the majority of men with erectile dysfunction (ED). However, many men with ED still report a suboptimal or partial response even after an adequate trial of oral PDE-5 therapy. Since ED is associated with impaired vascular function and both atorvastatin and quinapril have been previously shown to improve vascular function, we examined the effects of adjunctive treatment with these medications in men with vasculogenic ED who were suboptimal responders to 100 mg of sildenafil. Men with ED and suboptimal response to sildenafil were randomly assigned to 3 months of treatment with atorvastatin 40 mg (n = 12), quinapril 10 mg (n = 10), or placebo (n = 13), along with continued adjunctive sildenafil use. Measured variables included: International Index of Erectile Function (IIEF) questionnaire, brachial artery flow-mediated dilation (FMD), endothelium-independent dilation (EID) via nitroglycerin, penile Doppler blood flow, blood pressure (BP), lipids, and C-reactive protein (CRP). Compared to placebo, quinapril (p < 0.01) significantly improved symptoms of ED as measured by the IIEF-5 questionnaire. There was a trend toward a significant improvement in IIEF-5 with atorvastatin. Similarly, quinapril significantly improved the IIEF ED Domain (p < 0.05). Other peripheral and penile vascular parameters were unchanged with drug therapy as compared to placebo. In conclusion, treatment with quinapril, in combination with sildenafil, improved ED in men with suboptimal response to sildenafil alone. Atorvastatin demonstrated a trend toward improved ED in this group.

Oxidative stress and adverse adipokine profile characterize the metabolic syndrome in children.

Thirty-four children were assessed for body composition, blood pressure, lipids, glucose tolerance, markers of insulin resistance, oxidative stress, and adipokines. Children were divided into 3 groups: (1) normal weight, (2) overweight but otherwise healthy, and (3) overweight with the metabolic syndrome. There were no differences among any of the groups for age or Tanner stage, and anthropometric variables were similar between the overweight and the overweight with the metabolic syndrome groups. Differences across groups were found for high-density lipoprotein cholesterol (P < .001), triglycerides (P < .01), fasting insulin (P < .001), homeostasis model assessment (P < .01), adiponectin (P < .05), leptin (P < .0001), C-reactive protein (P < .0001), interleukin 6 (P < .0001), and 8-isoprostane (P < .001). In children, oxidative stress and adipokine levels worsen throughout the continuum of obesity and especially in the presence of components of the metabolic syndrome. Overweight children with components of the metabolic syndrome may be at elevated risk for future cardiovascular disease.

Comparison of B-mode and echo tracking methods of assessing flow-mediated dilation.

The aim of this study was to compare B-mode and echo tracking methods to assess endothelium-dependent flow-mediated dilation (FMD). Baseline brachial artery diameter, 60-s post cuff release diameter and FMD percent were assessed in 17 normal, healthy individuals using both techniques. Mean values for baseline diameter, 60-s diameter and FMD for M-mode were 3.83 +/- 0.69 mm, 4.06 +/- 0.66 mm and 6.35 +/- 3.98%, respectively. Mean values for baseline diameter, 60-s diameter and FMD for B-mode were 3.75 +/- 0.65 mm, 4.00 +/- 0.63 mm and 6.91 +/- 2.85%, respectively. Results, as displayed by Bland-Altman graphs, indicate a strong agreement between B-mode and echo tracking methods of assessing brachial artery diameter changes via FMD.

Inflammation, insulin, and endothelial function in overweight children and adolescents: the role of exercise.

OBJECTIVES: To assess subclinical inflammation, fasting insulin, and endothelial function before and after exercise in overweight children and adolescents. STUDY DESIGN: Twenty-five children (body mass index [BMI] >85th percentile) were assessed for brachial artery flow-mediated dilation (FMD), nitroglycerin-induced dilation, C-reactive protein (CRP), lipids, glucose, insulin, oral glucose tolerance, body composition, aerobic fitness (peak oxygen uptake [VO 2 peak]), and blood pressure. Twenty of these persons were equally and randomly assigned to either 8 weeks of stationary cycling or to a non-exercising control group. RESULTS: A baseline correlation was found between CRP and fasting insulin (r = 0.62; P < .001), which remained significant after adjusting for baseline variables (r = 0.53; P < .05). After 8 weeks, significant improvements were observed in the exercise group compared with the control group for VO 2 peak (exercise group = 21.8 +/- 2.1 to 23.2 +/- 1.5 mL/kg/minute vs control group = 23.4 +/- 1.6 to 20.9 +/- 2.2 mL/kg/minute; P < .05), high-density lipoprotein (HDL) cholesterol (exercise group = 1.02 +/- 0.03 to 1.10 +/- 0.04 mmol/L vs control group = 1.08 +/- 0.07 to 0.99 +/- 0.09 mmol/L; P < .05), and FMD area under the curve (AUC) (exercise group = 746 +/- 66 to 919 +/- 94 %*sec vs control group = 731 +/- 102 to 515 +/- 73 %*sec; P < .05). CONCLUSIONS: In overweight children and adolescents, CRP is independently associated with fasting insulin. Eight weeks of aerobic exercise improves fitness, HDL cholesterol, and endothelial function in this group.

Determinants of radial artery pulse wave analysis in asymptomatic individuals.

BACKGROUND: Noninvasive techniques to evaluate arterial stiffness include noninvasive radial artery pulse contour analysis. Diastolic pulse contour analysis provides a separate assessment of large (C1) and small artery (C2) elasticity. Analysis of the systolic pulse contour identifies two pressure peaks (P1 and P2) that relate to incident and reflected waves. This study aimed to compare indices from systolic and diastolic pulse contour analysis from the radial pressure waveform and to correlate these indices with traditional risk factors in asymptomatic individuals screened for cardiovascular disease. METHODS: In 298 consecutive subjects (206 male and 92 female healthy subjects with a mean age of 50 +/- 12 years), noninvasive radial artery pressure waveforms were acquired with a piezoelectric transducer and analyzed for 1) diastolic indices of C1 and C2 from the CR-2000 CVProfiler, and 2) systolic indices of augmentation as defined by augmentation pressure (AP), augmentation index (AIx), and systolic reflective index (SRI = P2/P1). These indices were then correlated to each other as well as to individual traditional risk factors and the Framingham Risk Score. RESULTS: Diastolic indices were significantly and inversely correlated to systolic indices with C2 showing a stronger inverse association than C1. C2 and Alx were significantly correlated with height, weight, and body mass index in men but not in women. All indices correlated better to blood pressure in women than men. In women, only systolic indices were significantly correlated to HDL cholesterol and only diastolic indices were significantly correlated to LDL cholesterol. All indices were significantly correlated to the Framingham Risk Score, which was stronger in women then men, but when adjusted for age only diastolic indices remained significant in women. CONCLUSIONS: Diastolic and systolic indices of pulse contour analysis correlate differently with traditional risk factors in men and women.

Detection of acute myocardial ischemia during percutaneous transluminal coronary angioplasty by endocardial acceleration.

The first heart sound is generated by vibrations from the myocardium during isovolumic contraction. Peak endocardial acceleration (PEA) has been used previously to measure these vibrations in humans and correlates with myocardial contractility during inotropic interventions. It is unknown if changes in PEA can be used to characterize a reduction in contractility during ischemic episodes. This study was designed to evaluate the use of an endocardial accelerometer for the detection of acute myocardial ischemia. Thirteen patients undergoing routine percutaneous transluminal coronary angioplasty (PTCA) consented to having a single-axis, lead-based accelerometer positioned in the right ventricular apex. PEA was defined as the maximum peak-to-peak amplitude during a window 50 ms before to 200 ms following the peak R wave. Time of endocardial acceleration (TEA) was defined as the time from the peak R wave to the maximum accelerometer signal within this window. To obtain a more robust estimate of the strength of vibrations, a 100-beat template of the accelerometer signal was constructed at baseline and applied as a matched filter during ischemia. The peak magnitude of the filtered endocardial accelerometer signal (Max Filtered EA) was used as an index of signal intensity. Median baseline PEA, TEA, and Max Filtered EA were 0.91 +/- 0.35 g, 75.2 +/- 16.2 ms, and 0.40 +/- 0.20 g, respectively. PEA and Max Filtered EA significantly decreased by 7% during ischemia (0.91 to 0.85 g and 0.40 to 0.37 g, both P < 0.05, respectively). TEA did not significantly change from baseline (77.0 ms, P = ns). The results of this study suggest that acute ischemia can be detected with an endocardial accelerometer in humans.

Impaired brachial artery endothelium-dependent and -independent vasodilation in men with erectile dysfunction and no other clinical cardiovascular disease.

OBJECTIVES: The goal of this study was to determine whether patients with vascular erectile dysfunction (ED) and no other clinical cardiovascular disease have structural and functional abnormalities of other vascular beds. BACKGROUND: In many ED patients, vascular disease is the major underlying cause. It may be that ED is an early marker of atherosclerosis in patients without clinical cardiovascular disease. METHOD: We assessed systemic vascular structure and function in 30 patients with ED and 27 age-matched normal control (NL) subjects. We measured vascular parameters, including: 1) carotid and brachial artery diameters, intima-media thickness, compliance, and distensibility; 2) aortic pulse wave velocity; 3) coronary calcification; and 4) brachial artery endothelium-dependent and -independent vasodilation. RESULTS: There were no significant differences in baseline demographics, coronary artery risk score, or lipid values between the two groups. Most structural and functional vascular parameters were similar in the ED and NL groups. Brachial artery flow-mediated vasodilation (FMD) (1.3 vs. 2.4%, p = 0.014) and vasodilation to nitroglycerin (NTG) (13.0 vs. 17.8%, p < 0.05) were significantly reduced in ED patients, compared with NL subjects. In addition, there was a significant correlation between FMD and vasodilation to NTG in ED patients (r = 0.59, p < 0.05) but not in NL subjects. CONCLUSIONS: Patients with ED but no clinical cardiovascular disease have a peripheral vascular defect in endothelium-dependent and -independent vasodilation that occurs before the development of other overt functional or structural systemic vascular disease and is independent of other traditional cardiovascular risk factors.

Clinical applications of arterial stiffness, Task Force III: recommendations for user procedures.

In vivo arterial stiffness is a dynamic property based on vascular function and structure. It is influenced by confounding factors like blood pressure (BP), age, gender, body mass index, heart rate, and treatment. As a consequence, standardization of the measurement conditions is imperative. General and method/device-specific user procedures are discussed. The subject's conditions should be standardized before starting measurements. These conditions include a minimal resting period of 10 min in a quiet room. It also includes prohibitions on smoking, meals, alcohol, and beverages containing caffeine before measurements. The position of the subject and time of measurements should be standardized. In comparative studies, corrections should be made for confounding factors. Repeated measurements are done preferably by the same investigator, and if available validated with user-independent automated procedures. As it is not feasible to discuss all methods or devices measuring arterial stiffness in one article, more attention is given to user procedures of commercially available devices, because these devices are of interest for a wider group of investigators. User procedures of methods/devices are discussed according to the nature of arterial stiffness measured: systemic, regional, or local arterial stiffness. Each section discusses general or method/device-specific user procedures and is followed by recommendations. Each recommendation discussed during the First International Consensus Conference on the Clinical Applications of Arterial Stiffness is quoted with the level of agreement reached during the conference. Also proposals for future research are made.