Left Ventricular Failure Group Research Articles

Vitamin D deficiency among patients with pulmonary hypertension

BackgroundThere is little information about vitamin D (Vit D) deficiency in patients with pulmonary hypertension (PH). The objective of this study was: 1) compare Vit D levels between patients with PH, left ventricular failure (LVF) and healthy subjects (HS); 2) correlate, in patients with PH, Vit D levels with prognosis-related variables, such as the 6-min walk test (6MWT).MethodsVitamin D levels were measured in a cross-sectional study in 126 patients from one of three groups: patients with PH (n = 53), patients with LVF (n = 42) and healthy subjects (n = 31). In all groups, 8-h fasting blood samples were obtained in the morning. In the PH and the LVF group, functional class (WHO criteria), metres covered in the 6MWT and echocardiographic parameters were analysed. In the PH group, plasma N terminal pro B type natriuretic peptide (NT-proBNP) level was analysed and a complete haemodynamic evaluation by right heart catheterisation was made.ResultsMean Vit D levels were lower in PH than in both other groups (ng/ml, mean ± SD): PH 19.25 ± 10, LVF 25.68 ± 12, HS 28.8 ± 12 (PH vs LVF p = 0.017, PH vs HS p = 0.001 and HS vs LVF p = 0.46). Vit D deficiency prevalence was higher in PH as compared to the other groups (PH 53.8%, LVF 45.2%, HS 25%, p = 0.01). Patients with PH in functional class (FC; WHO criteria) III–IV had higher Vit D deficiency prevalence than those in FC I–II (86.7% vs 40.5%, p = 0.003). There was a significant linear correlation between the 6MWT and Vit D levels in PH (p < 0.01), but not in LVF (p = 0.69).ConclusionsVit D levels were lower in patients with PH as compared to patients with LVF and HS and correlated directly with 6-min walk distance.

The Effect of Neurohormonal Blockade in Patients Supported with LVAD

Background: Neurohormonal blockade (NHB) is the mainstay of medical therapy for patients with heart failure with reduced ejection fraction. The role of NHB in patients with left ventricular assist devices (LVADs) is not well described. This study aims to assess the relationship between neurohormonal blockade and hemodynamics in LVAD patients. Methods: In this prospective study, LVAD patients undergoing a hemodynamic ramp study for speed optimization were enrolled. Complete hemodynamic data were collected at baseline prior to ramp study. Patients were divided into four groups: normal (central venous pressure (CVP) < 12 mmHg and pulmonary capillary wedge pressure (PCWP) < 18 mmHg), right ventricular failure (RVF) (CVP ≥ 12 and PCWP < 18), left ventricular failure (LVF) (CVP < 12 and PCWP ≥ 18), and biventricular failure (BiVF) (CVP ≥ 12 and PCWP ≥ 18). The use of beta blockers (BB), angiotensin converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARB), angiotensin receptor neprilysin inhibitors (ARNI) and aldosterone antagonists (AA) was compared across the groups. Categorical variables were compared using Chi-Squared Test and Fisher's Exact Test and continuous variables were compared using Independent T-tests and Mann-Whitney U Test. Results: Of 90 patients enrolled, 54 had normal hemodynamics, 10 had LVF, 11 had RVF, and 15 had BiVF. No intergroup differences were detected in the baseline characteristics, including gender, race, age, device type, and comorbidities. In the group with normal hemodynamics, 67% were taking ACEi or ARB, as compared to 33% in the BiVF group, 30% in the LVF group, and 73% in the RVF group (P = .02; Figure). AA, ARNI and BB use was not significantly different between the groups. Only a small percentage of patients in each group was on triple therapy with no significant intergroup differences. Among patients taking an ACEi/ARB, PCWP was 12.5 ± 5.6 vs 15.6 ± 6.0 mmHg for those not on ACEi/ARB (P = .01). There was no difference in mean arterial pressure (90 ± 11 vs. 89 ± 13 mmHg; P = .67) or CVP between these two groups (8.2 ± 4.7 vs. 9.9 ± 5.6 mmHg; P = .12). Conclusions: Greater ACEi/ARB use was observed in patients with normal hemodynamics and right heart failure as compared to those with elevated left-sided pressures. In addition, lower PCWP is seen in patients taking ACEi/ARB compared to those who are not. Further studies are warranted to evaluate the impact of medical therapy on LVAD outcomes.

Non-invasive method for rapid bedside estimation of inotropy: theory and preliminary clinical validation

BackgroundThere are numerous techniques which attempt to quantify inotropy (or myocardial contractility). None has yet found general acceptance in anaesthesia and critical care as a practical method. We report a novel approach to the determination of inotropy as a bedside procedure which could identify low inotropy states in patients with clinical heart failure. MethodsWe estimated the potential and kinetic energy delivered by the left ventricle using continuous-wave Doppler ultrasound (ultrasonic cardiac output monitor, Uscom, Sydney, Australia) and data available at the point of care. A formula to calculate effective inotropy [Smith-Madigan inotropy index (SMII)] was tested against historical haemodynamic data for 250 control subjects (ASA I patients from preoperative clinic) and 83 patients with acute left ventricular failure (LVF) of New York Heart Association Grade 4 (LVF group). The ratio of potential to kinetic energy (PKR) was investigated as a measure of arterial impedance. ResultsSignificant differences were found between the control and LVF groups for cardiac index, mean (range)=3.37 (2.84–5.32) vs 1.84 (1.43–2.26) litre min −1 m−2; stroke volume index (SVI), 49.2 (39–55) vs 34.3 (23–37) ml m−2; systemic vascular resistance, 893 (644–1242) vs 1960 (1744–4048) dyn s cm−5; SMII, 1.78 (1.35–2.24) vs 0.73 (0.43–0.97) W m−2; and PKR, 29:1 (24–35:1) vs 124:1 (96–174:1), P<0.001 in each case. Normal ranges were calculated for SMII and PKR as mean (+/−1.96) standard deviations, yielding 1.6–2.2 W m−2 for SMII, and 25–34:1 for PKR. ConclusionThe method clearly identified the two clinical groups with no overlap of data points. The discriminant power of SMII and PKR may offer valuable diagnostic methods and monitoring tools in anaesthesia and critical care. This is the first report of normal ranges for SMII and PKR.

Usefulness of right ventricular indices in early diagnosis of cardiac tamponade

Early diagnosis of postoperative cardiac tamponade is impeded by its clinical similarity to left ventricular failure. Moreover, the hemodynamic changes necessary to diagnose cardiac tamponade are detected by conventional monitoring technique only after clinical compromise. Early signs of cardiac tamponade and left ventricular failure were studied with emphasis on right ventricular function in anesthetized dogs. One group (n = 20) had cardiac tamponade produced by incrementally increasing pericardial pressure (2 to 20 mm Hg), and another group (n = 20) had acute left ventricular failure produced by successive ligation of the anterior descending coronary artery at the lower, middle, and upper thirds. Besides standard hemodynamic measurements, right ventricular function was examined with a rapid-response thermodilution catheter. During cardiac tamponade, cardiac output, right ventricular ejection fraction, right ventricular stroke volume, and right ventricular end-diastolic volume were significantly decreased from baseline values after a pericardial pressure of 8 mm Hg or more ( p < 0.05). Right atrial and pulmonary arterial pressures were not significantly elevated until 14 and 20 mm Hg of pericardial pressure, respectively. Although cardiac function in the left ventricular failure group was reduced after each ligation, right ventricular ejection fraction remained unchanged. This study suggests that right ventricular indices may facilitate earlier diagnosis of cardiac tamponade with greater accuracy.

Isoproterenol-induced alterations in myocardial blood flow, systolic and diastolic function in conscious dogs with heart failure.

The effects of isoproterenol were examined in 10 conscious, chronically instrumented adult dogs with left ventricular (LV) failure after pressure overload hypertrophy induced by aortic banding at 8-10 weeks of age (LV free wall plus septum-to-body weight ratio, 8.6 +/- 0.5 g/kg) and also in eight control dogs (LV free wall plus septum-to-body weight ratio, 5.1 +/- 0.3 g/kg). Baseline values of heart rate, LV end-diastolic pressure, LV end-diastolic stress, and LV systolic wall stress were greater in the LV failure dogs (p less than 0.01), whereas the ejection phase index, rate of change of LV short-axis diameter, LV dD/dt, was depressed compared with control animals. In the control animals, isoproterenol infusion increased Vcf and LV dD/dt significantly (p less than 0.05), whereas LV systolic wall stress did not change. In the LV failure dogs, the increases in Vcf and LV dD/dt were less (p less than 0.01), and LV systolic wall stress increased (p less than 0.01). In the control animals, LV end-diastolic pressure, LV end-diastolic stress, LV end-diastolic stress-dimension ratio, diastolic radial myocardial stiffness, and the time constant of isovolumic relaxation decreased (p less than 0.05), whereas in the LV failure dogs, LV end-diastolic pressure, LV end-diastolic stress, diastolic radial myocardial stiffness, and the LV end-diastolic stress-dimension ratio increased. In the LV failure group, the endocardial to epicardial blood flow ratio fell to 0.59 +/- 0.06 during isoproterenol infusion, that is, significantly lower than in control dogs (0.93 +/- 0.06). These data support the concept that potent sympathomimetic amines exert deleterious effects on systolic and diastolic function in the failing heart, potentially related to subendocardial hypoperfusion.

Circulation control of experimental and clinical profound left ventricular failures by automatic left ventricular assist system.

It is desirable that circulation control of the patient using a left ventricular assist device (LVAD) should be achieved appropriately and safely. We have developed an automatic LVAD system, which can maintain the normal circulation irrespective of the severity of heart failure and can restore the failing heart by decreasing the bypass flow (BF) through the LVAD as the heart recovers. The main part of the control-drive unit is an automatic level control (ALC) system for left atrial pressure (LAP) and total flow (TF). Profound left ventricular failure (LVF) was made by complete interception of blood supply to the extent of 50% (5 goats) and 70% (5 goats) of the LV free wall. The air-driven diaphragm-type LVAD was implanted between LA and aorta. At the beginning of LVAD pumping, BF tended to be very high to keep LAP at the preset level (0-5 mmHg) and to maintain TF at somewhat higher level (120-140 ml/kg/min). The recovering heart was able to decrease LAP gradually. Since the LAP was set at a certain level, the ALC of LAP decreased BF to maintain LAP at the preset level. During the recovering stage from LVF, preset level of LAP was gradually raised while checking the pulmonary function. When natural heart output exceeded 100 ml/kg/min, LVAD was removed. The 50% LVF group recovered between 17 hours and 3 days, and 70% LVF group between 6th and 16th postoperative day. This LVAD system was then applied to the postoperative profound LVF in a MVR patient whose entire circulation was maintained normal during 14 day pumping. The failed heart gradually recovered and the pump was successfully removed. We consider that the decompression of LV will prevent overextension of impaired myocardium and simultaneously accelerate the solid scar formation. And gradual increase of LV work will promote the compensation ability of the residual myocardium. Continuous LVAD assistance can therefore earn time for the impaired myocardium to recover while maintaining normal circulation.

Serial M-mode echocardiography in severe chronic aortic regurgitation.

Thirteen patients with severe chronic aortic regurgitation (mean age 52.5 years) were studied by serial M-mode echocardiography. When first studied, none had breathlessness caused by left ventricular failure (LVF). Nine of these patients remained asymptomatic over a mean period of 4 years, 3 months (no LVF group); the other four patients developed left ventricular failure with dyspnea after a mean interval of 3 years, 11 months (LVF group). For both of these groups, we compared the echocardiographic measurements from the first and last of the serial studies. For the LVF group, end-diastolic left ventricular internal dimension increased 14%, end-systolic dimension increased 35%, fractional shortening decreased 45% and left atrial dimension increased 62%. All of these changes were significant. For the No LVF group, the change in end-diastolic left ventricular internal dimension was not significant, but the 6% increase in end-systolic dimension, 10% reduction in fractional shortening and 25% increase in left atrial size were all statistically significant. Although echocardiography could detect declining left ventricular function in a group of asymptomatic patients with severe chronic aortic regurgitation, the reproducibility of the technique was limited in individual patients. Therefore, serial echocardiographic studies should be interpreted in conjunction with clinical assessment and other investigations.