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Cardiovascular disease (CVD) in the HIV population accounts for a large proportion of morbidity and mortality and, with the increased life expectancy, the burden of CVD is expected to rise. Inflammation, immune dysfunction, side effects of HIV medications, high prevalence of other risk factors are the likely pathogenic mechanisms for accelerated atherosclerosis. We aimed to evaluate the diagnostic yield of a cardiovascular multimodality diagnostic work-up in a contemporary cohort of HIV-infected patients. From November 2017 to October 2019, HIV infected patients were screened in a cardiovascular diagnostic work-up program including clinical history, physical examination, arterial blood pressure measurement, 12-lead ECG, and Transthoracic Echocardiogram (TTE). Advanced non-invasive cardiovascular imaging tests, like Coronary Computed Tomography Angiography (CCTA), stress-echocardiography, Cardiac Magnetic Resonance (CMR), were performed in patients with suspicion of chronic coronary syndrome (CCS) or non-ischemic heart disease (NIHD). 117 HIV-infected consecutive patients underwent this cardiovascular diagnostic work-up and were included in our study. Fifty-two patients (45%) had evidence of CVD. Of them, 22 presented Coronary Artery Disease (CAD), whereas 47 cases showed NIHD. In 17 cases both conditions were present. Among patients with CAD, 8 showed critical coronary stenosis; among them, 5 were treated with percutaneous coronary intervention, 2 with Aorto-Coronary By-Pass Grafting (CABG), and one with medical therapy. Hypertension and diabetes were significantly associated with the development of CVD (respectively p<0.001 and p< 0.05), while current smoking (p<0.02) and hypertension (p<0.007) were positively associated to CAD. A comprehensive cardiovascular diagnostic work-up including advanced multimodality diagnostic imaging modalities led to early detection of CVD in nearly half of an HIV population with immediate interventions required in 6.8% of them, and aggressive prevention treatment started in the remaining HIV patients.

Background: Aortic prosthesis area (EOA) is computed by continuity equation from left ventricular (LV) stroke volume (SV) derived from LV outflow tract diameter (LVOT D ) or, when unmeasurable, from LV volumes (SV V ). There is evidence to suggest LVOT ellipticity and recommend 3D LVOT area (LVOT CSA ) adoption in aortic stenosis. We sought to evaluate if the same concept applies to supra-annular aortic prosthesis comparing SV and EOA derived from LVOT D (EOA D ) and from LVOT CSA (EOA CSA ). EOA computed from SV V (EAO V ) accuracy was evaluated in this setting. Patient-prosthesis mismatch (PPM) was compared among different EOA computations., Methods: A consecutive series of 202 patients (aged 81 ± 4 years, 43% males) underwent St.Jude Trifecta aortic valve replacement (AVR) and were followed up with echocardiography at one-year (335 ± 31 days). All measurements followed the EACVI or ASE guidelines, 3D X-plane modality was used to compute SVv and measure LVOT CSA ; SV was calculated from LVOT D (SV D ) and LVOT CSA (SV CSA ). PPM was indexed EOA <0.65 cm²/m²., Results: LVOT showed a significant ellipticity index (1.17 ± .27), independent of prosthesis size. EOA D (1.70 ± 0.55 cm²) was less than EOA CSA (1.95 ± 0.62 cm²) (P < .0001). SV V was significantly lower than SV D and SV CSA . Bland-Altman analysis showed a significant correlation between SV V and SV D or SV CSA although with large bias and imprecision. The correlations improved reducing bias and imprecision when LVOT time-velocity integral was <20 cm. PPM incidence was higher in EOA V (15.6%) compared to EOA D (P = .04) or EOA CSA (P < .001)., Conclusions: In supra-annular AVR, LVOT retains its elliptical shape and LVOT CSA yielded larger prosthesis EOA with lower PPM incidence. PPM may be overestimated by EOA V ., (© 2017, Wiley Periodicals, Inc.)

Objective: To study the sequence of atrial activation and the interatrial electromechanical delay (IEmD) noninvasively in healthy subjects during sinus rhythm (SR).Methods and Results: In 66 SR healthy subjects P-wave activation was analyzed by means of vectorcardiography. The timing of atrial contractions was measured as the intervals between the P-wave and the A-wave of the Doppler right and left ventricular inflows (P-A(t) and P-A(m)), and IEmD was calculated as the algebraic difference P-A(m)- P-A(t). In the horizontal plane the vectorcardiographic P-loop was anteroposterior ("typical", 41 subjects), anterior (18), or posterior (7). IEmD (mean +/- SE 17 +/- 8 ms) was directly related to R-R and P-R intervals. IEmD was significantly shorter in anterior and posterior P loops than in the typical (6.5 +/- 5.3 and 8.1 +/- 10.1, respectively, vs 24.2 +/- 3.1 ms). In the posterior P-loop group, who exhibited longer P-A(t), mitral E-wave velocity and E/A ratio were reduced, and left atrial booster function was increased.Conclusion: IEmD was widely variable in SR, reflecting the origin site of sinus impulse, which independently influenced ventricular filling dynamics. [ABSTRACT FROM AUTHOR]

Background: Because of the shortage of donor hearts, the criteria for acceptance have been considerably expanded. Abnormal results on pharmacologic stress echocardiography are associated with significant coronary artery disease and/or occult cardiomyopathy on verification by cardiac autopsy. The aim of this study was to establish the feasibility of an approach based on pharmacologic stress echocardiography as a gatekeeper for extended heart donor criteria., Methods: From April 2005 to April 2010, 39 "marginal" candidate donors (mean age, 56 ± 6 years; 21 men) were initially enrolled. After legal declaration of brain death, marginal donors underwent rest echocardiography, and if the results were normal, dipyridamole (0.84 mg/kg over 6 min, n = 25) or dobutamine (up to 40 μg/kg/min, n = 3) stress echocardiography., Results: A total of 19 eligible hearts were found with normal findings. Of these, three were not transplanted because of the lack of a matching recipient, and verification by cardiac autopsy showed absence of significant coronary artery disease or cardiomyopathy abnormalities. The remaining 16 eligible hearts were uneventfully transplanted in marginal emergency recipients. All showed normal (n = 14) or nearly normal (minor single-vessel disease in two) angiographic, intravascular ultrasound, hemodynamic and ventriculographic findings at 1 month. At follow-up (median, 14 months; interquartile range, 4-31 months), 14 patients survived and two had died, one at 2 months from general sepsis and one at 32 months from allograft vasculopathy in recurrent multiple myeloma., Conclusions: Pharmacologic stress echocardiography can safely be performed in candidate heart donors with brain death and shows potential for extending donor criteria in heart transplantation., (Copyright © 2011 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.)

Background: The hyperdynamic circulation of hepatic cirrhosis is related to decreased systemic vascular resistance due to arterial vasodilation. Urotensin II plasma levels are increased in cirrhotic patients, and have been suggested to play a role in the pathogenesis of systemic haemodynamic alterations., Aim: To evaluate the relationships between systemic haemodynamics and urotensin II plasma levels., Methods: Thirty-six consecutive in-patients with cirrhosis and no alteration of plasma creatinine, and 20 age- and gender-matched healthy volunteers underwent noninvasive assessment of systemic haemodynamics and measurement of urotensin II plasma levels., Results: In comparison to healthy controls, cirrhotic patients had signs of hyperdynamic circulation and higher plasma urotensin II levels. Plasma urotensin II was neither significantly different amongst patients with different severity of cirrhosis nor between patients with or without ascites. Both in controls and cirrhotic patients no significant correlations were found between parameters of systemic haemodynamics and plasma urotensin II levels., Conclusions: In patients with cirrhosis and hyperdynamic circulation, but with normal serum creatinine, urotensin II is higher than in healthy subjects. However, no correlation with cardiac index or other haemodynamic parameters was observed, indicating that other mechanisms prevail., (Copyright © 2010 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.)

Aims: To investigate whether and how cold pressor test (CPT) could affect myocardial perfusion and left ventricular (LV) function in patients with previous LV ballooning syndrome (LVBS)., Methods and Results: Cold pressor test (3 min hand immersion in ice-water) was performed in 17 women with previous LVBS and in 7 age- and risk factor-matched women with chest pain and normal coronary arteries. At baseline and peak CPT, global and regional LV function, and myocardial perfusion were quantitatively assessed by real-time three-dimensional echocardiography (RT3DE) and myocardial contrast (SonoVue, Bracco) 2D echocardiography (MCE), respectively (Philips iE33 machine, X3-1 and S5-1 probes). Data were analysed off-line (QLab 6.0 software). Peripheral venous catecholamines were assayed by high performance liquid chromatography with electrochemical detection. Cold pressor test induced similar haemodynamic changes and catecholamine increase in controls and LVBS patients. Left ventricular ejection fraction decreased and transient new mid-ventricular and apical motion abnormalities developed in LVBS patients only (quantitative RT3D analysis), without corresponding perfusion defects (MCE). At peak CPT, coronary blood flow and velocity increased (quantitative MCE analysis) in control subjects only., Conclusion: Cold pressor test induced LV wall motion abnormalities unmatched to regional coronary flow reduction in LVBS patients only. The reduced coronary reserve in response to CPT suggests microvascular dysfunction in LVBS patients.

Objectives: To evaluate the effects of primary coronary angioplasty (PCA) on regional left ventricular (LV) contractile dysfunction and deformation, and on global remodeling., Methods: In 99 consecutive patients (81 males, aged 61+/-11 years) who underwent successful PCA of left anterior descending (LAD) and right coronary (RCA) arteries for treatment of first myocardial infarction and completed a hemodynamic follow-up at 1 and 6 months, LV eccentricity and circularity indexes, centreline wall motion and regional curvature were analyzed. Asynergy and akinesia were defined as centreline impairment -1 standard deviation) at 6 months was used to categorize the outcome as improved., Results: Systolic deformation and impairment of regional LV function soon after LAD and RCA occlusion closely resembled those of the chronic myocardial infarction. PCA improved regional contractility in all patients, due to early salvage of the epicardial injured myocardium, and at least in two fifths of patients the injury area magnitude reduced by improvement of the ischemic boundaries of the infarct. Irrespective of either persistently impaired or normalized regional contractility, LV shape remained abnormal. In contract to the persistence of local deformation, global remodeling was observed in patients categorized as the highest end-diastolic volume quartile at presentation who had greater myocardial damage., Conclusion: Regional contractility impairment induced by acute myocardial infarction can be reverted by PCA, but systolic shape deformation persists over time.

Introduction: Patients with hypertrophic cardiomyopathy (HCM) are at risk for lethal ventricular arrhythmia, but the electrophysiological substrate behind this is not well-understood. We used non-invasive electrocardiographic imaging to characterize patients with HCM, including cardiac arrest survivors. Methods: HCM patients surviving ventricular fibrillation or hemodynamically unstable ventricular tachycardia (n = 17) were compared to HCM patients without a personal history of potentially lethal arrhythmia (n = 20) and a pooled control group with structurally normal hearts. Subjects underwent exercise testing by non-invasive electrocardiographic imaging to estimate epicardial electrophysiology. Results: Visual inspection of reconstructed epicardial HCM maps revealed isolated patches of late activation time (AT), prolonged activation-recovery intervals (ARIs), as well as reversal of apico-basal trends in T-wave inversion and ARI compared to controls (p < 0.005 for all). AT and ARI were compared between groups. The pooled HCM group had longer mean AT (60.1 ms vs. 52.2 ms, p < 0.001), activation dispersion (55.2 ms vs. 48.6 ms, p = 0.026), and mean ARI (227 ms vs. 217 ms, p = 0.016) than structurally normal heart controls. HCM ventricular arrhythmia survivors could be differentiated from HCM patients without a personal history of life-threatening arrhythmia by longer mean AT (63.2 ms vs. 57.4 ms, p = 0.007), steeper activation gradients (0.45 ms/mm vs. 0.36 ms/mm, p = 0.011), and longer mean ARI (234.0 ms vs. 221.4 ms, p = 0.026). A logistic regression model including whole heart mean activation time and activation recovery interval could identify ventricular arrhythmia survivors from the HCM cohort, producing a C statistic of 0.76 (95% confidence interval 0.72-0.81), with an optimal sensitivity of 78.6% and a specificity of 79.8%. Discussion: The HCM epicardial electrotype is characterized by delayed, dispersed conduction and prolonged, dispersed activation-recovery intervals. Combination of electrophysiologic measures with logistic regression can improve differentiation over single variables. Future studies could test such models prospectively for risk stratification of sudden death due to HCM. [ABSTRACT FROM AUTHOR]

There are several well-known medical conditions in which posture and gravity interact with natural history, including pregnancy. In this review, we provide a comprehensive overview of interactions between maternal posture and maternal physiology and pathophysiology at rest during pregnancy. We conducted a systematic literature search of the MEDLINE database and identified 644 studies from 1991 through 2021, inclusive, that met our inclusion criteria. We present a narrative review of the resulting literature and highlight discrepancies, research gaps, and potential clinical implications. We organize the results by organ system and, commencing with the neurological system, proceed in our synthesis generally in the craniocaudal direction, concluding with the skin. The circulatory system warranted our greatest and closest consideration-literature concerning the dynamic interplay between physiology (heart rate, stroke volume, cardiac output, blood pressure, and systemic vascular resistance), pathophysiology (e.g., hypertension in pregnancy), and postural changes provide an intricate and fascinating example of the importance of the subject of this review. Other organ systems discussed include respiratory, renal, genitourinary, gastrointestinal, abdominal, and endocrine. In addition to summarizing the existing literature on maternal posture-physiology interactions, we also point out gaps and opportunities for further research and clinical developments in this area. Overall, our review provides both insight into and relevance of maternal posture-physiology interactions vis à vis healthcare's mission to improve health and wellness during pregnancy and beyond. [ABSTRACT FROM AUTHOR]

Background: We sought to analyze the characteristics of local left ventricular deformation related to functional mitral regurgitation (MR) in post-anterior myocardial infarction scar, and to evaluate how local remodeling contributes to late development of MR after surgical ventricular reconstruction by endoventricular circular patch plasty repair., Methods: Two hundred twenty-one consecutive patients (aged 60 +/- 9 years; 193 males) with previous transmural anterior infarction underwent heart catheterization both before and 1 year after endoventricular circular patch plasty repair. Preoperative global left ventricular shape determinants (eccentricity and circularity indexes), regional curvature and wall motion (centerline), and both preoperative and 1-year postoperative hemodynamic parameters (volumes, ejection fraction, capillary wedge and pulmonary artery pressures) were calculated., Results: Forty-eight patients had (MR patients), and 173 did not have (NoMR patients) angiographic MR grade 2 or more preoperatively; at follow-up, 30 NoMR patients had MR (late MR [LMR]). Before surgery, MR patients had larger left ventricular volumes, higher capillary wedge and mean pulmonary artery pressures, and lower ejection fraction and cardiac index. The LMR patients had similarly high capillary wedge and pulmonary artery pressures as MR patients; otherwise, they did not differ from NoMR patients. Mitral regurgitation patients had wider lateral wall akinesia and greater inferior wall asynergy; the inferobasal region was hypokinetic in LMR patients. In MR patients, inferior wall systolic curvature was less negative; the inferobasal region had a more positive curvature in LMR patients., Conclusions: Local deformation of the inferior wall with loss of systolic inward bending is associated with functional MR, while asynergy and systolic deformation of the inferobasal region and high capillary wedge pressure are prognostic signs of MR development late after endoventricular circular patch plasty repair.

Risk stratification of chest pain (CP) is still debated. Objective of this study was to evaluate the performance of a risk stratification model for patients with suspected acute coronary syndrome (ACS) and nondiagnostic ECG at presentation, in whom the occurrence of myocardial infarction was either diagnosed following traditional (t-MI) or the recently redefined (r-MI) criteria. First-line 6-h work-up categorized 3068 patients with suspected ACS and nondiagnostic ECG into low-risk for short-term coronary events, intermediate-risk who entered second-line work-up, and high-risk. Intermediate-risk patients with positive second-line work-up and high-risk patients were considered for urgent coronary angiography. Angina, non-fatal MI, sudden death, and revascularization constituted composite end-point (CE) for in-hospital and 6-month outcome. ACS incidence was 16%; r-MI increased by 62% the diagnosis of MI over t-MI. Among 2024 discharged low-risk patients, 12 (0.6%) had non-fatal CE at 6 months. ACS was diagnosed in 19% of 503 intermediate-risk and 96% of 389 high-risk patients. Among ACS patients, in-hospital CE occurred in 14% of t-MI, 7% of r-MI, and 9% of unstable angina (UA) patients (t-MI vs. r-MI and t-MI vs. UA: p<0.05, for both); 6-month CE occurred in 23%, 16% and 12% of t-MI, r-MI and UA, respectively (t-MI vs. UA: p<005). Sensitivity, specificity and accuracy were high both for diagnostic (97%, 98%, 99%, respectively) and treatment (83%, 98%, 97%, respectively) strategy. Risk stratification, and categorization according to traditional or redefined MI and UA criteria allow safe allocation of resources in CP patients with suspected ACS and nondiagnostic ECG at presentation because outcome is accurately predicted.

Background: Electrophysiological abnormalities underlying the increased arrhythmogenicity of left ventricular hypertrophy (LVH) are still under investigation. The aim of this study was to assess non-invasively the electrophysiologic alterations in two different types of LVH, METHODS: Multiparametric non-invasive ECG analysis (R-R interval, QRS and QT intervals, QT dispersion, T-wave complexity, activation-recovery interval [ARI] dispersion, standard deviation of RR intervals [SDNN], filtered QRS duration [fQRS], root-mean-square voltage of the terminal 40 ms of the fQRS [RMS40] and low amplitude signal duration (< 40 microV) in the terminal portion of the fQRS [LAS]) was performed in 57 patients with hypertensive LVH and hypertrophic cardiomyopathy (HCM), and in 105 healthy subjects., Results: The R-R interval and SDNN were similar in hypertrophic patients and controls. QRS and QT intervals were longer in hypertrophic patients without any differences between hypertensive LVH and HCM. QT dispersion, T-wave complexity and fQRS were greater in hypertrophic patients; QT dispersion was the greatest in HCM. ARI dispersion was lesser in hypertrophic patients without any differences between subgroups of LVH. fQRS showed a trend toward higher values in hypertensive patients. LAS at 25 Hz had a trend toward lower values in HCM patients, while LAS at 40 Hz and RMS40 showed no difference between controls and hypertrophic patients. Left ventricular mass index was not correlated with any of the above-mentioned parameters., Conclusions: The QT interval and dispersion did not identify the type of hypertrophy. Similarly, ARI dispersion which explores local variations of repolarization duration, and T-wave complexity could not distinguish patients with hypertensive LVH from those with HCM indicating that multiparametric ECG data are affected more by the presence of LVH, than by its type.

Background: Ventricular repolarization abnormalities can represent a trigger for lethal arrhythmias in hypertrophic cardiomyopathy (HCM). We sought to assess whether multiparametric computerized surface ECG analysis identifies repolarization abnormalities in HCM patients, and whether this approach allows identification of patients with syncope., Methods: In 28 HCM patients and 102 healthy subjects (14 and 51 males, mean age 44 +/- 15 and 41 +/- 14 years, respectively), 8-lead ECG (I, II, V1-V6) was recorded for 5 min, acquired in digital format and analyzed. Heart-rate corrected QT (QTc) and T wave complexity index (TWCc), QT dispersion, activation-recovery interval (ARI) and its dispersion, signal duration in the terminal portion of the filtered QRS at 25 Hz (LAS(25 Hz)) were analyzed among other parameters., Results: Compared to healthy subjects, HCM patients exhibited longer QRS, filtered QRS, QTc and QTd, greater TWCc, minor ARId and LA(25 Hz). QRS duration and maximal septum thickness were linearly correlated (r=0.231 p<0.001). ARId shortening depended on ARI shortening in lead V1 (241 +/- 51 vs. 287 +/- 45, HCM vs. healthy subjects, p<0.0001) and lengthening in V6 (257 +/- 42 vs. 209 +/- 34, HCM vs. healthy subjects, p<0.0001). Significant factors for syncope at Wilks' stepwise discriminant analysis were TWCc, QRSd and LAS(25 Hz) (F=14.394, 10.098 and 9.226, respectively) with 92.3% positive predictive accuracy., Conclusions: In HCM, longer QRS and QT intervals are consequences of increased left ventricular mass, while ARI seems to reflect myocardial activation rather than inhomogeneity of recovery. The simultaneous evaluation of TWC, QRSd and LAS(25 Hz), unable by itself to hold a predictive value, yielded high accuracy in predicting cardiogenic syncope., (Copyright 2004 Elsevier Ireland Ltd.)

In patients with cirrhosis and portal hypertension, standing induces a reduction in cardiac index (CI) and an increase in systemic vascular resistance index. Our previous studies indicate that this abnormal hemodynamic response to standing is due to an altered myocardial function, because cirrhotic patients are unable to compensate for the reduced preload with an increase in left ventricular (LV) ejection fraction (EF) and stroke volume. To evaluate whether the cardiac dysfunction in cirrhosis is influenced by canrenone, an aldosterone antagonist, 8 patients with preascitic, nonalcoholic cirrhosis, and portal hypertension underwent echocardiographic assessment of LV function and systemic hemodynamics and determinations of plasma volume, urinary sodium excretion, and plasma renin activity (PRA), aldosterone (PAC), and norepinephrine (PNE) when on a 150-mmol/d-sodium diet (baseline), after 1 month on canrenone (100 mg/d) plus a 40-mmol/d-sodium diet and after 1 month on canrenone plus a 150-mmol/d-sodium diet. Echocardiographic evaluation was performed with the patient in the supine position and during active standing. At baseline, patients had high plasma volume and normal renal function, PRA, PAC, and PNE. CI, LVEF, and stroke volume index were also normal. Standing caused a significant reduction in CI and LVEF. After canrenone and either sodium diet, CI significantly decreased, and PRA and PNE increased in the supine position. On standing, LVEF and CI did not decrease further. Plasma volume significantly decreased only after low-sodium diet plus canrenone. In conclusion, canrenone normalizes the cardiac response to the postural challenge in patients with preascitic cirrhosis.

Background: Sudden cardiac death represents a major public health problem, but in the general population the identification of those subjects at very high risk remains poor. Simultaneous multiparametric ECG analysis can improve the identification of high-risk patients., Methods: Five-min ECG recordings at a 5 MHz sampling rate (extended length-XL-ECG, Mortara Instruments, Milwaukee, WI, USA) were acquired in 105 healthy subjects (age range 21 to 80 years), equally distributed for age decades and sex, and three additional recordings, 30 min apart, were repeated in 30 subjects on the second day. The following parameters were recorded and analyzed: the RR interval, QRS duration, QT interval corrected according to the Bazett and Fridericia formulae, QT dispersion, T wave complexity, activation-recovery interval dispersion, standard deviation of the RR intervals, filtered QRS duration, the square root of the mean voltage of the last 40 ms of the filtered QRS, and the length of time that the terminal vector magnitude complex remains < 40 microV., Results: QRS duration, activation-recovery interval dispersion, and filtered QRS differed in the two sexes. The standard deviation of the RR intervals, T wave complexity and QT dispersion were significantly correlated with age. The reproducibility was good for each parameter., Conclusions: The XL-ECG allows the simultaneous calculation of eight adequately reproducible different parameters the values of which are in agreement with those of the literature. Thus, XL-ECG is a reliable time- and cost-saving tool.

To assess whether an increased production of nitric oxide is involved in the circulatory and renal alterations of cirrhosis, we evaluated systemic hemodynamics (echocardiography), renal hemodynamics, and sodium handling (lithium clearance method), plasma renin activity (PRA), aldosterone (PAC), and norepinephrine in 7 patients (3 men, mean age 65 +/- 2 years) with compensated cirrhosis, portal hypertension, and hyperdynamic circulation during intravenous N(G)-monomethyl-L-arginine (L-NMMA) (3 mg/kg bolus plus 0.05 mg/kg. min for 120 minutes) or placebo (the vehicle) in a randomized, placebo-controlled, crossover study. Administration of L-NMMA resulted in significant reductions in plasma and urinary nitrite levels and plasma cyclic guanosine monophosphate (cGMP), indicating effective inhibition of nitric oxide synthase. L-NMMA also significantly reduced cardiac index (-13%) and increased systemic vascular resistance (+26%), arterial pressure (+9%), renal blood flow (+12%), glomerular filtration rate (+12%), and sodium excretion (+25%). Changes in sodium excretion were caused by both enhanced filtered sodium load and reduced sodium reabsorption in the proximal tubule. Plasma norepinephrine significantly decreased in response to L-NMMA, and there was a trend for reductions in PRA and PAC. Placebo had no appreciable effect on any of the measured parameters. These results indicate that in patients with compensated cirrhosis, portal hypertension and hyperdynamic circulation inhibition of nitric oxide synthase corrects the altered systemic hemodynamics and improves renal function and sodium excretion.

Objective: To evaluate the cardiovascular response to active postural changes in pregnancy., Design: Prospective study., Setting: Outpatient Clinic, Fetal Maternity Unit., Participants: Sixteen healthy women referred prior to pregnancy., Methods: Heart rate, arterial pressure, echocardiographic end-diastolic and end-systolic left ventricular volumes (Teichholz' s formula) were measured in the three months before pregnancy, at the end of the first and second trimester, at mid third trimester, and six months after delivery in the supine and standing position, in thirteen women (mean age 33, range 25-38 years)., Results: Cardiac output (supine position) significantly increased (28%): it reached its maximum at the second trimester, remained steadily elevated in the mid third trimester, and returned to baseline after delivery. Cardiac output increased during pregnancy also in the active orthostatic position, the percentage increase being greater (70%) since the standing pre-conception value was lower. The postural stress induced similar changes in heart rate, arterial pressure and left ventricular ejection fraction before, during and after pregnancy. However, the reduction in cardiac output associated with early standing attenuated significantly at the second trimester and it was absent at mid third trimester (F = 3.13, P = 0.021). This was due to the interplay between the significantly lesser increase in systemic vascular resistance, occurring since the first trimester, and the significantly lesser decrease in left ventricular end-diastolic volume which was observed in the mid third trimester., Conclusion: These data indicate that the elevated cardiac output is adequately maintained in pregnancy during the postural challenge, due to optimisation of the responses of preload and afterload.

The cardiovascular effects of low-dose adrenomedullin (ADM, 1, 2 and 3 pmol kg-1 min-1 for 30 min each) were evaluated in six healthy subjects in a placebo controlled, cross-over study by determining cardiac volumes, systolic and diastolic function (echocardiography) and systemic haemodynamics before, during and after ADM or placebo. High-resolution ultrasound was used to evaluate changes in carotid artery distension. ADM caused a +85% increment in its plasma levels and significantly increased plasma cyclic adenyl monophosphate (cAMP). Compared with placebo, ADM induced significant decrements in left ventricular (LV) systolic diameter and systemic vascular resistance, and increments in LV posterior wall thickening, ejection fraction and cardiac index. Right and left atrial emptying fraction and carotid artery distention increased. LV diastolic function, heart rate, and plasma renin activity did not change, whereas packed cell volume increased. These results indicate that ADM influences cardiovascular function and systemic haemodynamics at physiological plasma levels in man mainly because of its vasodilating activity, leading to reduced afterload.

The aim of the study was to evaluate: 1) the cardiovascular function and the autonomic drive to the heart in patients affected by primary hyperparathyroidism (pHPT) with no evidence of renal and cardiovascular complications; 2) the cardiovascular effects of acute administration of PTH in normal subjects. In 14 patients affected by mild asymptomatic pHPT echocardiographic assessment of cardiovascular function and of the mechanic properties of the brachial and carotid artery, heart rate variability and the dispersion of QT interval were performed before and 6 months after successful surgery. Twenty age- and sex-matched healthy subjects were included in the study. Five healthy volunteers underwent a single blind, placebo-controlled, random order, cross-over study with infusion of PTH (hPTH 1-34, 200 U in saline over 5 min) or placebo. Echocardiographic assessment of cardiovascular function, heart rate variability, and QT interval were performed between 20 and 25 min after the start of the infusion and repeated after 15 min of tilting at 60 degrees. In pHPT patients the echocardiographic parameters were normal; left ventricular isovolumetric relaxation time was always in the normal range, but significantly shorter than in control subjects, suggesting an increased sympathetic stimulation. Arterial diameters and thickness, blood pressure, and QT interval were not significantly different with respect to normal subjects and were unchanged 6 months after surgery. pHPT patients lacked the circadian rhythm of the low frequency to high frequency ratio, suggesting an increased sympathetic drive to the heart at nighttime. In normal subjects there were no significant differences in basal echocardiographic measurements during PTH infusion with respect to placebo and in the hemodynamic response to tilt. These results suggest that cardiovascular function is substantially normal in normotensive pHPT patients with mild hypercalcemia. A modulation of the adrenergic control of circulation seems to be associated with hypercalcemia and/or chronic PTH excess, but its biological relevance needs further investigations.

Background/aims: The aim of this study was to evaluate cardiovascular and renal function in patients with compensated cirrhosis and essential hypertension in the supine position and in response to standing up., Methods: Twenty-four patients with compensated cirrhosis (12 with elevated arterial pressure) and 20 healthy volunteers underwent echocardiographic evaluation of left ventricular end-diastolic and stroke volumes, ejection fraction, cardiac index, arterial pressure, peripheral resistance, creatinine clearance and sodium excretion in both the supine and the standing position., Results: When supine, only normotensive patients had a hyperdynamic circulation, with increased left ventricular end-diastolic and stroke volumes, cardiac index, and ejection fraction, and reduced peripheral resistance. Creatinine clearance and sodium excretion were comparable in patients and controls. Standing induced a decrease in end-diastolic volume in all subjects. Healthy volunteers maintained cardiovascular homeostasis by increasing ejection fraction and heart rate, while both normotensive and hypertensive cirrhotic patients experienced a fall in stroke volume and cardiac index, despite a marked activation of the renin-aldosterone and sympathetic nervous system. Creatinine clearance decreased only in normotensive patients, who experienced the greatest reduction in sodium excretion., Conclusions: Compensated cirrhotic patients with arterial hypertension had no evidence of hyperdynamic circulation. Like their normotensive counterparts, hypertensive patients had an impaired cardiovascular response to the postural challenge, but a lesser degree of renal dysfunction during standing.

We evaluated cardiac function and the plasma levels of atrial (ANP) and brain (BNP) natriuretic peptides during bicycle (B) and hand-grip (HG) exercises in eight healthy males. Each test was preceded by a control protocol in resting conditions. Left ventricular (LV) function (echocardiography) was evaluated during both exercises. Atrial function was assessed only during HG. Plasma ANP significantly increased during B (+236%) and HG (+77%), while there was a significant trend towards higher plasma BNP levels during B (+41%) and HG (+30%) than during the corresponding control tests. Plasma ANP correlated with heart rate in both tests, with left atrial volume, pulmonary vein flow systolic fraction and mitral flow E/A ratio in HG; BNP in both test correlated with LV dimensions and function. These data suggest that during exercise the cardiac release of ANP and BNP is differently regulated and related to changes in left atrial and LV function, respectively.

The influence of age, sex, left ventricular hypertrophy (LVH) and geometry on the autonomic activity to the heart was investigated in 96 hypertensive out-patients (53 men, mean age 53 +/- 9 years) and 39 healthy subjects (19 men, mean age 43 +/- 1 years). Using 24-h Holter recordings, time [the standard deviation of all RR intervals (SDNN) and the square root of the mean of the squared differences between adjacent normal RR intervals (RMSSD)] and power spectral analysis of RR intervals [Fast Fourier algorithm, low/high frequency (LF/HF) ratio] were calculated over 24 h, daytime (D) and nighttime (N) periods in all subjects. Signal averaged electrocardiogram was recorded in 50 patients to detect late potentials. Stepwise multiple linear regression analysis showed that the 24-h LF/HF ratio was influenced by age and sex, D-LF/HF by age and N-LF/HF by sex, a higher LF/HF ratio being found in younger patients and in men. These data suggest a more prominent sympathetic modulation of cardiac activity in these groups. No differences in RR period variations were observed between patients with or without LVH. Late potentials were observed in 10 patients, and did not correlate with any of the measured parameters.

Few data have been published about the relation between the vessels geometry and development of left ventricular (LV) hypertrophy in patients with arterial hypertension. The aim of this study is to describe arterial and LV geometry changes due to mild-to-moderate arterial hypertension in an untreated hypertensive population. In 95 untreated patients with mild-to-moderate hypertension and 23 age- and sex-matched healthy normotensives, we measured the end-diastolic diameter and wall thickness of the left ventricle and the internal diameter and intimal-medial thickness (IMT) of carotid and brachial arteries. From these data, the cross-sectional areas (CSAs) of arterial and myocardial walls were calculated. Hypertensive patients were further subdivided on the basis of the presence of LV hypertrophy defined according to Devereux et al as anatomical LV mass >125 g/m. In hypertensive patients with hypertrophy, carotid and brachial CSAs increased, without significant changes in thickness/diameter ratio (arterial 'enlargement'), while the left ventricle developed 'concentric' hypertrophy. Arterial and LV CSAs showed a significant direct correlation with systolic blood pressure (BP). However, when data were corrected for BP, the correlation between the increase in arterial and LV CSAs became much improved than for the raw data. In conclusion patients with untreated mild-to-moderate hypertension, both carotid and brachial arterial walls showed an enlargement that was proportional to the development of LV hypertrophy. These results suggest that the effects of arterial hypertension on carotid, brachial and LV wall geometry have a common modulation.

Background/aims: Patients with cirrhosis and ascites usually show alterations of systemic hemodynamics and are thus prone to develop arterial hypotension, which might result in cerebral hypoperfusion if cerebral autoregulation is impaired., Methods: We evaluated cerebral autoregulation in 15 patients with cirrhosis and ascites and 15 healthy subjects by monitoring mean blood flow velocity in the middle cerebral artery and arterial pressure during supine rest and passive tilting., Results: Tilt provoked a drop of arterial pressure in both groups. Control subjects had a prompt recovery of mean flow velocity and a progressive recovery of arterial pressure, so that, after 120 s, both parameters had returned to baseline: at 20 s the recovery of flow velocity was faster (p<0.01) than that of blood pressure. By contrast, patients with cirrhosis had a delayed and incomplete recovery of both parameters (p<0.01 vs healthy subjects). In eight patients, the recovery of mean flow velocity paralleled that of arterial pressure, indicating an impaired cerebral autoregulation. These patients had a worse liver function, a higher cardiac index and lower peripheral resistance., Conclusions: Cerebral autoregulation is often impaired in patients with cirrhosis and ascites. These patients can develop cerebral hypoperfusion if arterial pressure falls abruptly.

At the onset of wall motion alterations during dobutamine echocardiographic stress testing, a steeper increase in the overall T-wave amplitude in the precordial leads was observed in 17 patients with baseline normal wall motion, electrocardiogram, and critical coronary stenoses compared with 11 control subjects. Eleven patients with increasing T-wave amplitude had localized apical dyssynergy, whereas 6 patients with downward displacement of the ST segment had widespread wall motion alterations also located at the basal and midsegments.

We evaluated the cardiovascular effects of pathophysiological plasma levels of brain natriuretic peptide in seven patients with mild to moderate essential hypertension by performing equilibrium radionuclide angiocardiography at baseline and during brain natriuretic peptide infusion at increasing doses (4, 8, 10, and 12 pmol/kg per minute for 20 minutes each). Brain natriuretic peptide induced a progressive reduction of left ventricular end-diastolic volume (from 107.5 +/- 10.3 to 89.0 +/- 11.0 mL at the end of all infusion periods) and end-systolic volume, whereas stroke volume did not show any significant change (from 64.9 +/- 5.9 to 62.7 +/- 7.8 mL). Cardiac output, arterial pressure, and peripheral vascular resistance did not change significantly. The lack of effects on systemic hemodynamics was probably due to compensatory activation of the sympathetic nervous system, as indicated by the significant increase in plasma norepinephrine levels (from 1.75 +/- 0.18 to 2.19 +/- 0.21 nmol/L), heart rate (from 68 +/- 6 to 81 +/- 6 beats per minute), peak ejection rate, and peak filling rate. These results indicate that brain natriuretic peptide, at the pathophysiological plasma concentrations reached in this study, influences cardiovascular homeostasis mainly by reducing cardiac preload.