Mean Pulmonary Wedge Pressure Research Articles

Abstract 11006: Prevalence and Hemodynamic Profiles of Pulmonary Hypertension in Cardiac Amyloidosis

Background: While cardiac amyloidosis (CA) classically involves the left ventricle (LV), less is known about its impact on the right ventricle (RV) and pulmonary vasculature. Objectives: We aimed to determine the prevalence and types of PH profiles in CA, and to determine hemodynamic and cardiovascular magnetic resonance (CMR) predictors of major adverse cardiovascular events (MACE). Methods: CA patients who underwent CMR and right heart catheterization (RHC) from 2010-2019 were included. Patients were assigned the following hemodynamic profiles: no PH, pre-capillary PH, isolated post-capillary PH (IPCPH), or combined pre- and post-capillary PH (CPCPH). Transpulmonary gradient (TPG)—the difference between mean pulmonary artery and wedge pressures, was calculated. The relationship between PH profile and MACE (death, heart failure hospitalization) was assessed using survival analysis. CMR and RV parameters were correlated with MACE using Cox-Regression analysis. To evaluate the importance of parameters for predicting MACE, Random Forest algorithm for survival analysis were applied. Results: A total of 52 patients were included (age 69±9 years, 85% male, 60% transthyretin, and 40% light chain CA). PH was present in 50 (96%) patients. RHC was performed during biopsy in 44(85%) and for clinical indications in 8(15%) patients. Rates of no PH, pre-capillary PH, IPC-PH, and CPCPH were 5(10%), 3(6%), 29(55%) and 15(29%) respectively (Panel A). Hemodynamic PH profile did not correlate with death (p=0.98) or MACE (p=0.67) (Panel B). TPG (HR 0.88, CI 0.80-0.97), RV, (HR 0.95, CI 0.92-0.98), and LV ejection fraction (HR 0.95, CI 0.92-0.98) were significantly associated with MACE. In Random Forest analysis, LVEF, RVEF, and TPG were the most important predictors of MACE (Panel C). Conclusions: PH is highly prevalent in CA, even at the time of diagnosis. While IPC-PH was most common, CPCPH is not infrequent. TPG and RVEF are prognostic markers in this population.

Hemodynamic Response to Acute Volume Load in Heart Transplant Recipients

A mean pulmonary wedge pressure (mPAP) ≥ 25 mm Hg following volume load or exercise has been proposed as a partition value for detection of HfpEF. However, the hemodynamic response to volume challenge in heart transplant (Tx) recipients has never been studied. 36 heart Tx recipients (Age: 65 years) with normal LV function (EF: 55 ± 7 %) and without rejection and graft vasculopathy underwent right heart catheterization to measure hemodynamic response to volume loading before and after a rapid saline infusion of 7mL/kg over 10 min. PCWP, right atrial pressure (RAP), mean pulmonary artery pressure(PA) were obtained and the PCWP and indexed(i) stroke volume(SV) data were used to construct Starling (SVindex/PCWP) curves. Pts were categorized in those with elevated filling pressures (Group DD, n=10 pts) defined by a PCWP ≥ 15 mm Hg at rest or ≥ 25 mm Hg following volume loading vs those without (Controls, n=26 pts). No difference in age of donor and transplant, baseline hemodynamics and EF was noted between both groups. Saline infusion significantly increased PCWP and mean PA in both Groups without any significant change in BP and heart rate. Interestingly saline infusion was associated with a significant rise in SV and SVi in Controls not in DD pts(Fig 1). Moreover, in DD pts the Starling curves revealed a larger SVi at any give PCWP compared to Controls pts. In the transplanted heart volume loading increases filling pressures and is able to unmask left ventricular diastolic dysfunction. Interestingly, those with DD are characterized by a blunted Frank Starling response as evidenced by higher PCWP and failure to increase SV for any given PCWP. Further prospective studies are warranted to unravel the underlying mechanisms.

The value of assessing femoral vein to femoral artery ratio in the treatment of patients with heart failure

Objective: To investigate the relationship between ultrasound derived ratio of femoral vein to femoral artery diameter and hemodynamics in patients with heart failure. Methods: This was a case-control study. A total of 61 patients with heart failure and 49 patients with non-heart failure hospitalized in the Department of Critical Care Medicine from September 2017 to September 2018 were included in this study. Doppler ultrasound was used to measure the femoral artery and vein diameter. After deep inhalation, the femoral vein diameter was measured again, and the ratio of femoral vein and artery diameter was calculated. The central venous pressure (CVP) and mean pulmonary wedge pressure (mPAWP) were also measured. Pearson correlation analysis was used to explore the correlation between the ratio of femoral vein diameter to femoral artery diameter and CVP and mPAWP, and linear regression equation was established. Results: The overall CVP and mPAWP levels were significantly higher, and the femoral vein diameter after deep inhalation was bigger in heart failure patients than in non-heart failure patients(all P<0.001). The femoral vein diameter/femoral artery diameter ratio was positively correlated with CVP (r=0.76, P<0.001), and positively correlated with mPAWP (r=0.40, P<0.001) in heart failure group. The linear regression equation established by the femoral vein/femoral artery diameter ratio and CVP in the heart failure group showed that the inner diameter of the femoral vein/the inner diameter of the femoral artery ratio≥1.3 corresponded CVP≥15.518 cmH2O(1 cmH2O=0.098 kPa) in heart failure patients. Conclusions: In patients with heart failure, the inner diameter of the femoral vein/femoral artery ratio is positively correlated with CVP and mPAWP. The ratio of inner diameter of the femoral vein/femoral artery can be used to assess the volumetric load of patients with heart failure and to guide the clinical treatment of heart failure patients.

Impact of hypothermia on cardiac performance during targeted temperature management after cardiac arrest

IntroductionTargeted temperature management (TTM) is a well-accepted neuro-protective intervention in the management of comatose survivors of cardiac arrest (CA). However, the impact of TTM on cardiac performance has not been adequately evaluated. MethodsWe reviewed data on consecutive CA survivors undergoing TTM at a quaternary cardiac intensive care unit between January 2015 and June 2017. Enrollment was restricted to cases with invasive hemodynamics (iHDs) at TTM initiation, every 8 h at target temperature (32–34 °C) and at completion of rewarming (>36 °C), unless precluded by mortality. Cardiac index and cardiac index-derived variables were adjusted for a decreased oxygen consumption during hypothermia. We assessed the serial impact of cooling on iHDs and cardiac performance utilizing longitudinal data analysis accounting for the effects of time as surrogate for the expected change from the post arrest syndrome and instituted treatments. A Frank–Starling construct was used to evaluate changes in cardiac contractility. ResultsWe evaluated the effects of cooling on iHDs and cardiac performance in 46 CA survivors. Heart rate decreased with cooling (p < 0.001), to return to baseline after rewarming (p = 0.6). Mean arterial pressure and pulmonary wedge pressure decreased by cooling (p < 0.001 for both), with sustained improvement after rewarming (p < 0.001 for both). Systemic vascular resistance was unaffected by hypothermia (p > 0.05). Left stroke work index increased with cooling (p < 0.001), with return to baseline after rewarming (p = 0.6). Cooling was associated with a left-upward shift in the Frank–Starling curve indicative of increased contractility. ConclusionMild hypothermia in CA survivors appears associated to positive changes in iHDs and cardiac performance, including a potential increase in cardiac contractility. Larger studies are needed to conclusively confirm these findings.

Abstract 17278: Concomitant Use of Ivabradine in the Setting of Cardiogenic Shock: A Case Series

Background: Ivabradine, a selective sinus node inhibitor, is indicated for patients with chronic heart failure with reduced ejection fraction (HFrEF). Use in cardiogenic shock is currently contraindicated. However, studies have suggested increasing heart rate may be deleterious for patients with HFrEF due to an inverted Bowditch-Treppe response. Limited case series have suggested use of Ivabradine in decompensated HFrEF may be beneficial. We present a case series of patients who presented with severely decompensated HFrEF and received inotropic support and concomitant ivabradine. Methods: We selected four patients with HFrEF presenting with elevated sinus heart rate and cardiogenic shock (cardiac index &lt;2.0L/min*m2with pulmonary artery wedge pressure &gt; 20 mmHg by invasive hemodynamic monitoring) while on inotropic therapy and were intolerant of beta blockade due to hypotension. Ivabradine 2.5 mg 12 h was initiated and subsequently titrated with continued monitoring with baseline, 24 h and latest obtained parameters recorded. Other treatments occurred at the discretion of the attending physician. Results: Four male patients (mean age 44 years) with non-ischemic cardiomyopathy (mean EF 17%, mean NT-pro-BNP 5104 pg/ml) were included. Ivabradine was tolerated in all cases, with a mean dose of 6 mg q12h. Mean heart rate and pulmonary wedge pressure fell 20% and 32% respectively from baseline to last measurement, while stroke volume increased with an overall improvement in cardiac index. (Table 1) There were no changes noted in mean arterial blood pressure. All patients underwent successful wean of inotropic support within 48 hours and were discharged alive on beta blocker and ACE inhibitor therapy. No adverse events attributed to use of Ivabradine were observed. Conclusion: In our small series of patients with cardiogenic shock, beta blocker intolerance and elevated sinus heart rate, Ivabradine was added without any deleterious hemodynamic effect and associated with early clinical improvement. Further studies are needed to better assess its potential use in this population.

Effect of Exercise on Pulmonary Arterial Capacitance in Heart Failure

PURPOSE: Heart failure is often associated with abnormal pulmonary hemodynamics. Pulmonary arterial capacitance (PAC) is a measure of the distensibility of the pulmonary vasculature and is a determinant of right ventricular afterload. Previously it has been shown that, at rest, PAC demonstrates a hyperbolic relationship with pulmonary vascular resistance (PVR) in heart failure (HF) patients and is an independent predictor of mortality. Our aim was to determine how exercise affects PAC and its relationship with exercise capacity and indices of respiratory gas exchange. METHODS: 39 HF patients undergoing right heart catheterization performed incremental exercise to exhaustion. Pulmonary arterial systolic pressure (PAPs), pulmonary arterial diastolic pressure (PAPd), mean pulmonary artery pressure (PAPm), and mean pulmonary wedge pressure (PWPm) were measured invasively at rest and at peak exercise. Ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), and heart rate (HR) were continuously collected at rest and during exercise. Arterial and mixed venous blood samples were collected for determination of cardiac output (Q) via direct Fick. The following variables were then calculated: stroke volume (SV)=Q/HR; PAC=SV/(PAPs-PAPd); PVR=(PAPm-PWPm)/Q. RESULTS: PAC significantly decreased from rest to peak exercise (2.6 vs. 1.6 ml/mmHg, p<0.01). At peak exercise, PAC was correlated with VO2max (PAC=0.29*VO2max-0.87, R=0.74). PAC was negatively correlated to PVR at rest (R=0.85) and during exercise (R=0.82) according to a hyperbolic fit. PAC was negatively correlated to VE/VCO2 at rest (R=0.53) and during exercise (R=0.52) according to a hyperbolic fit. CONCLUSIONS: In patients with classic systolic HF, PAC is reduced and falls further with exercise. In addition, subjects with the greatest capacitance to accept increases in pulmonary blood volume have a better exercise capacity. This increased pulmonary vascular distensibility during exercise yields lower resistance to forward flow. The gas exchange measure ventilatory efficiency, a marker of disease severity and prognosis in HF patients, is also related to reduced PAC. Supported by NIH grant HL71478.

Evaluation of bilateral pulmonary artery banding for initial palliation in single-ventricle neonates and infants: risk factors for mortality before the bidirectional Glenn procedure.

Bilateral pulmonary artery banding is considered as 'first-stage' palliation for neonates who have hypoplastic left heart syndrome. This study aimed to identify risk factors that influence outcome before the bidirectional Glenn operation. This retrospective evaluation involved 30 consecutive patients with hypoplastic left heart syndrome, or a variant, who underwent bilateral pulmonary artery banding between August 2005 and December 2011 at our institution. Clinical echocardiographic, operative and catheter examination data were reviewed. This study included 9 patients with hypoplastic left heart syndrome and 21 patients with variants. Bilateral pulmonary artery banding was performed at a median age of 7 days. Finally, 19 patients had the bidirectional Glenn operation performed (Group A), and the remaining 11 patients died before the bidirectional Glenn procedure (Group NA). Catheter evaluations before the bidirectional Glenn procedure were carried out at 97 ± 34 days. The mean pulmonary venous wedge pressure was significantly lower (Group A: 13.1 ± 3.1 mmHg vs Group NA: 22.9 ± 3.7 mmHg, P <0.01), systemic ventricular ejection fraction was higher (54.4 ± 10.7 vs 41.7 ± 9.9%, P <0.05), systemic ventricular end-diastolic pressure was lower (6.1 ± 2.4 vs 10.5 ± 3.6 mmHg, P <0.05) and the rate of patients with more than mild systemic atrioventricular valve regurgitation was lower in Group A than in Group NA (15.7 vs 62.5%, P <0.05). Multivariate logistic regression analysis showed that mean pulmonary venous wedge pressure was the most significant predictor of attaining the bidirectional Glenn anastomosis (odds ratio: 2.35, P <0.01). Postoperative atrioventricular valve regurgitation, cardiac function and mean pulmonary venous wedge pressure are closely correlated with mortality after bilateral pulmonary artery banding. Additional treatments, including operations, are considered to maintain cardiac function and not to raise pulmonary venous wedge pressure before the bidirectional Glenn procedure.

Accuracy of chest radiography in predicting pulmonary hypertension: A case-control study

To assess the accuracy of chest radiography (CXR) in predicting pulmonary hypertension (PH). We studied 108 consecutive patients with suspected PH who underwent right heart catheterization (RHC). All were PH treatment naives. Hemodynamic criteria included a mean pulmonary artery pressure >25 mmHg at rest, and a mean pulmonary wedge pressure <15 mmHg. Postero-anterior and lateral CXR were obtained shortly before RHC. To avoid a selection bias which could be introduced by examining only patients with suspected PH, we included in the analysis the CXR of 454 additional patients with different diagnosis: 57 with left heart failure (LHF) and pulmonary venous hypertension at RHC, 197 with chronic obstructive pulmonary disease, and 200 non-obstructed controls. CXR were examined independently by 4 raters, who were blinded to clinical, hemodynamic, and spirometric data. The diagnosis of PH was made if a prominent main pulmonary artery was associated with anyone of: isolated enlargement of right ventricle, right descending pulmonary artery >16 mm in diameter, pruning of peripheral pulmonary vessels. Eighty-two patients had PH confirmed at RHC. Weighted sensitivity of CXR was 96.9% (95% confidence interval, 94.9 to 98.2%), and weighted specificity 99.8% (95% confidence interval, 99.6 to 99.9%). By considering the 165 patients who underwent RHC, weighted sensitivity of CXR was unchanged, and weighted specificity decreased to 99.1%. None of the patients with PH were misclassified as having LHF, and vice versa. CXR is accurate in predicting PH. It may aid clinicians in selecting patients with suspected PH for hemodynamic ascertainment.

Cardiorenal Outcomes After Slow Continuous Ultrafiltration Therapy in Refractory Patients With Advanced Decompensated Heart Failure

The purpose of this study was to examine the clinical outcomes of using slow continuous ultrafiltration (SCUF) in patients with acute decompensated heart failure (HF) refractory to intensive medical therapy. Several studies have demonstrated the clinical usefulness of early SCUF in patients with acute decompensated HF to improve fluid overload and hemodynamics. We reviewed clinical data from 63 consecutive adult patients with acute decompensated HF admitted to the Heart Failure Intensive Care Unit from 2004 through 2009 who required SCUF because of congestion refractory to hemodynamically guided intensive medical therapy. The mean creatinine level was 1.9 ± 0.8 mg/dl on admission and 2.2 ± 0.9 mg/dl at SCUF initiation. After 48 hours of SCUF, there were significant improvements in hemodynamic variables (mean pulmonary arterial pressure: 40 ± 12 mm Hg vs. 33 ± 8 mm Hg, p = 0.002, central venous pressure: 20 ± 6 mm Hg vs. 16 ± 8 mm Hg, p = 0.007, mean pulmonary wedge pressure: 27 ± 8 mm Hg vs. 20 ± 7 mm Hg, p = 0.02, Fick cardiac index: 2.2 l/min/m(2) [interquartile range: 1.87 to 2.77 l/min/m(2)] vs. 2.6 l/min/m(2) [interquartile range: 2.2 to 2.9 l/min/m(2)], p = 0.0008), and weight loss (102 ± 25 kg vs. 99 ± 23 kg, p < 0.0001). However, there were no significant improvements in serum creatinine levels (2.2 ± 0.9 mg/dl vs. 2.4 ± 1 mg/dl, p = 0.12) and blood urea nitrogen (60 ± 30 mg/dl vs. 60 ± 28 mg/dl, p = 0.97). Fifty-nine percent required conversion to continuous hemodialysis during their hospital course, and 14% were dependent on dialysis at hospital discharge. Thirty percent died during hospitalization, and 6 patients were discharged to hospice care. In our single-center experience, SCUF after admission for acute decompensated HF refractory to standard medical therapy was associated with high incidence of subsequent transition to renal replacement therapy and high in-hospital mortality, despite significant improvement in hemodynamics.

Effects of Phosphodiesterase Type 5 Inhibition on Systemic and Pulmonary Hemodynamics and Ventricular Function in Patients With Severe Symptomatic Aortic Stenosis

Pressure overload resulting from aortic stenosis causes maladaptive ventricular and vascular remodeling that can lead to pulmonary hypertension, heart failure symptoms, and adverse outcomes. Retarding or reversing this maladaptive remodeling and its unfavorable hemodynamic consequences has the potential to improve morbidity and mortality. Preclinical models of pressure overload have shown that phosphodiesterase type 5 inhibition is beneficial; however, the use of phosphodiesterase type 5 inhibitors in patients with aortic stenosis is controversial because of concerns about vasodilation and hypotension. We evaluated the safety and hemodynamic response of 20 subjects with severe symptomatic aortic stenosis (mean aortic valve area, 0.7 ± 0.2 cm(2); ejection fraction, 60 ± 14%) who received a single oral dose of sildenafil (40 or 80 mg). Compared with baseline, after 60 minutes, sildenafil reduced systemic (-12%; P<0.001) and pulmonary (-29%; P=0.002) vascular resistance, mean pulmonary artery (-25%; P<0.001) and wedge (-17%; P<0.001) pressures, and increased systemic (13%; P<0.001) and pulmonary (45%; P<0.001) vascular compliance and stroke volume index (8%; P=0.01). These changes were not dose dependent. Sildenafil caused a modest decrease in mean systemic arterial pressure (-11%; P<0.001) but was well tolerated with no episodes of symptomatic hypotension. This study shows for the first time that a single dose of a phosphodiesterase type 5 inhibitor is safe and well tolerated in patients with severe aortic stenosis and is associated with improvements in pulmonary and systemic hemodynamics resulting in biventricular unloading. These findings support the need for longer-term studies to evaluate the role of phosphodiesterase type 5 inhibition as adjunctive medical therapy in patients with aortic stenosis.

Hemodynamic and Neurochemical Determinates of Renal Function in Heart Failure

In patients with chronic heart failure (HF) abnormalities in renal function are common and have a strong negative impact on prognosis. The etiology of renal dysfunction in HF is poorly understood. We measured systemic blood pressure, central hemodynamics, GFR (inulin), renal plasma flow (RPF, para-amino hippurate) and renal sympathetic activity (radiotracer assessment of transrenal norepineprine gradient corrected for extraction) in 62 patients with NYHA class II-III HF secondary to LV systolic dysfunction. Mean age was 58±11 years and the mean EF was 25±7%. Regression analysis revealed that GFR was systematically related to RPF, right atrial pressure and mean arterial BP but not to mean pulmonary artery pressure, wedge pressure cardiac output, EF or measures of renal sympathetic activity. Multiple regression analysis revealed that the only independent predictor of GFR was RPF. Further regression analysis revealed that RPF was systematically related to renal sympathetic activity, right atrial pressure, and wedge pressure but not mean arterial BP, cardiac output or EF. Multiple regression analysis revealed that only right atrial independently predicted RPF. Hemodynamic, neurochemical and renal function responses to Dobutamine (n=13) and Nitroprusside (n=23) were evaluated. Changes in GFR in response to these interventions were closely correlated with changes in right atrial, mean pulmonary artery and wedge pressure but not to changes in cardiac output, systemic arterial BP or renal sympathetic activity. In this case the multiple regression analysis revealed that decreases in right atrial and wedge pressures were both independent predictors of increases in GFR. These data support the concept that GFR is strongly dependent on RPF, which, in turn, is independently related to right atrial pressure. Further, reductions in right and left heart filling pressures in response to therapeutic interventions independently predict increases in GFR. These findings suggest that reductions in cardiac filling pressure should continue to be an important goal in the management of chronic HF while modifications of cariac output and systemic arterial pressure appear to have less impact on renal function.

Correlation of central venous–arterial and mixed venous–arterial carbon dioxide tension gradient with cardiac output during neurosurgical procedures in the sitting position

The study was conducted to evaluate the correlation of central venous-arterial and mixed venous-arterial pCO(2) gradient with cardiac output in patients being operated in the sitting position. Fifty-one patients, aged 41-69 years, classified as American Society of Anesthesiologists physical status II and III, scheduled to undergo elective neurosurgical procedures in the sitting position, were enrolled in this prospective cohort study. Simultaneous blood gas samples from arterial, central venous and pulmonary artery catheters were collected at four different time points during supine and sitting position. Cardiac index (CI) determination was accomplished simultaneously, with continuous cardiac output technique. The mixed venous-arterial pCO(2) and central venous-arterial pCO(2) gradients were calculated and related to CI at the specific time points, thus a total of 204 points of comparison were obtained. Changing from the supine to the sitting position induced a significant deterioration of CI, right atrial pressure, mean pulmonary arterial pressure and pulmonary wedge pressure. The mean delta pCO(2) difference (bias) in the four time points ranged between -0.07 and -0.27. The upper (1.59-1.71 mmHg) and lower limits of agreement (-2.16 to -1.82 mmHg) were quite narrow, suggesting an acceptable overall agreement between the mixed and central venous pCO(2) differences. The coefficient of determination (R(2)) between the venous-arterial pCO(2) and CI for mixed and central venous circulations was 0.830 and 0.760 (P < 0.001 for both), respectively. In contrast, R(2) values between mixed and central venous oxygen saturation values and CI were 0.324 and 0.286, respectively (P < 0.001 for both), illustrating a rather weak relationship. It seems that venous-arterial pCO(2) values obtained from mixed and central venous circulations can be reliably interchanged in estimating CI in patients undergoing neurosurgical procedures in the sitting position. Thus, central venous-arterial pCO(2) gradient could serve as a useful and simple method for estimating cardiac performance, in which further invasive monitoring is not strongly indicated.

Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography

The assessment of left ventricular (LV) diastolic function should be an integral part of a routine examination, particularly in patients presenting with dyspnea or heart failure. About half of patients with new diagnoses of heart failure have normal or near normal global ejection fractions (EFs). These patients are diagnosed with “diastolic heart failure” or “heart failure with preserved EF.”1 The assessment of LV diastolic function and filling pressures is of paramount clinical importance to distinguish this syndrome from other diseases such as pulmonary disease resulting in dyspnea, to assess prognosis, and to identify underlying cardiac disease and its best treatment. LV filling pressures as measured invasively include mean pulmonary wedge pressure or mean left atrial (LA) pressure (both in the absence of mitral stenosis), LV end-diastolic pressure (LVEDP; the pressure at the onset of the QRS complex or after A-wave pressure), and pre-A LV diastolic pressure (Figure 1).Although these pressures are different in absolute terms, they are closely related, and they change in a predictable progression with myocardial disease, such that LVEDP increases prior to the rise in mean LA pressure. Figure 1 The 4 phases of diastole are marked in relation to high-fidelity pressure recordings from the left atrium (LA) and left ventricle (LV) in anesthetized dogs. The first pressure crossover corresponds to the end of isovolumic relaxation and mitral valve opening. In the first phase, left atrial pressure exceeds left ventricular pressure, accelerating mitral flow. Peak mitral E roughly corresponds to the second crossover. Thereafter, left ventricular pressure exceeds left atrial pressure, decelerating mitral flow. These two phases correspond to rapid filling. This is followed by slow filling, with almost no pressure differences. During atrial contraction, left atrial pressure again exceeds left ventricular pressure. The solid arrow points to left ventricular minimal pressure, the dotted arrow to left ventricular …

Waon therapy for chronic heart failure: a novel innovative therapy

We developed a form of Waon therapy [1] in which the entire body is warmed in an evenly heated chamber for 15 minutes at 60oC that soothes the mind and body, and after the deep-body temperature has increased by 1.0−1.2oC, the soothing warm effects are sustained by maintaining the warmth at rest for an additional 30 minutes. Regarding the acute effects of Waon therapy, we demonstrated that it improved acute hemodynamics in patients with chronic heart failure (CHF), including cardiac index, mean pulmonary wedge pressure, systemic and pulmonary resistance, and cardiac function. We had already performed Waon therapy for several hundred patients with CHF due to dilated or ischemic cardiomyopathy and confirmed that this therapy decreased the death or re-hospitalization in comparison to non-Waon therapy patients. We conducted a prospective multi-center study to confirm the effect of Waon therapy on CHF at 10 participating hospitals. Two weeks of Waon therapy improved NYHA classification, and significantly decreased the cardiac size on both the chest X-ray and echo findings. Echocardiography demonstrated a significant improvement in cardiac function, and serum levels of brain natriuretic peptides and noradrenalin decreased after two weeks of Waon therapy. In order to clarify the mechanism of the effect of Waon therapy, we analyzed the vascular endothelial function and reported that two-week Waon therapy significantly improved endothelial function in patients with CHF. Furthermore, we performed experimental studies using TO-2 cardiomyopathic hamsters, and noticed that repeated Waon therapy increased mRNA and protein of endothelial nitric oxide synthase (eNOS) in TO-2 hamsters. This therapy also improved survival in TO-2 cardiomyopathic hamsters without any pharmacological treatments. In conclusion, Waon therapy is a novel, safe, cost-effective and innovative therapy for patients with CHF.

Hemodynamic and Exercise Performance With Pulsatile and Continuous-Flow Left Ventricular Assist Devices

Continuous-flow rotary pumps with axial design are increasingly used for left ventricular assist support. The efficacy of this design compared with pulsatile, volume displacement pumps, with respect to characteristics of left ventricular unloading, and exercise performance remains largely unstudied. Thirty-four patients undergoing implantation with a pulsatile, volume displacement pump operating in a full-to-empty cycle (HeartMate XVE; Thoratec Inc, Pleasanton, Calif; n=16) or continuous-flow rotary pump with an axial design operating at a fixed rotor speed (HeartMate II; Thoratec Inc; n=18) were evaluated with right heart catheterization and echocardiography preoperatively and at 3 months postoperatively and cardiopulmonary exercise testing 3 months postoperatively. Support with either the XVE or II resulted in significant (P<0.05) increases in cardiac output and reduction in mean pulmonary artery and pulmonary wedge pressures. Exercise capacity at 3 months was similar between groups (% predicted peak VO2-XVE: 46.8+/-10.2 versus II: 49.1+/-13.6). Echocardiography at 3 months demonstrated a significantly (P<0.05) greater reduction in left ventricular end-diastolic volume (-49+/-16% versus -35+/-20%), left ventricular end-systolic volume (-59+/-20 versus -37+/-21%), and percent mitral valve regurgitant volume (-99+/-2% versus -52+/-56%) for the XVE compared with II, respectively. The HeartMate XVE or II provided equivalent degrees of hemodynamic support and exercise capacity. The XVE was associated with greater left ventricular volume unloading. Characteristics of left ventricular pressure and volume unloading between these pump designs and mode of operation do not influence early exercise performance.

Intravenous Esmolol is Well Tolerated in Elderly Patients with Heart Failure in the Early Phase of Non-ST Elevation Myocardial Infarction

To investigate the haemodynamic response to and clinical safety and tolerability of intravenous esmolol (Brevibloc), Baxter Healthcare Corporation, Deerfield, Illinois, USA) in elderly and younger patients with acute non-ST elevation myocardial infarction (NSTEMI) and heart failure. We studied 24 consecutive patients, 12 of them elderly (> or =75 years old) and 12 younger (32-74 years old), with NSTEMI and symptoms of heart failure on presentation. After stabilisation of the patient's condition with standard therapy, intravenous esmolol was administered. An infusion rate of 0.05 mg/kg/min for 30 minutes was instituted and, if no adverse effects developed, this was increased to 0.20 mg/kg/min. All haemodynamic parameters were measured before and at the end of each administration using a Swan-Ganz catheter. Only one patient in the elderly subgroup did not tolerate the augmented infusion rate (because of severe bradycardia) and so had to return to the initial lower infusion rate. The cardiac index (mean +/- SD) was 2.4 +/- 0.9 L/min/m(2) at baseline and decreased to 1.9 +/- 0.4 L/min/m(2) (p < 0.05 vs baseline) at the end of the administration of the second dose of esmolol in the elderly patients and 2.6 +/- 0.5 L/min/m(2) and 2.2 +/- 0.5 L/min/m(2) (p < 0.05 vs baseline), respectively, in the younger patients. Mean pulmonary wedge pressure was 17 +/- 6mm Hg at baseline and increased to 19 +/- 4mm Hg (p < 0.05 vs baseline) at the end of the second dose of esmolol in the elderly patients and 16 +/- 10mm Hg and 18 +/- 10mm Hg (p < 0.05 vs baseline), respectively, in the younger patients. The response of both age groups to esmolol was the same for all of the parameters examined. Intravenous esmolol was safe and well tolerated in the early phase of NSTEMI in patients presenting with symptoms of heart failure and ongoing ischaemia, regardless of their age.

557 Tissue and functional abnormalities of the myocardium in patients with hypertrophic cardiomyopathy and cardiac arrest: a strain-strain rate and integrated backscatter study

and hemodynamic assessment. Results: Out ol the 38 pts. (mean age: 594-12 years) 24 had CP, and 14 RCM; 20 pts. (53°/°) had sinus rhythm, and 18 (47%) atrial fibrillation. Mean pulmonary wedge pressure (PCW) was 21 4-6 mmHg, E was 1054-39 cm/s, deceleration time of E was 1414-37 ms without a significant difference between RCM and CR Mean pulmonary arterial pressure (PAP) was 284-8 mm Hg with a significant dilference between RCM and CP (334-10 vs. 264-4 mm Hg; p 8 crn/s in 20/24 CP pts (83%). The 4 CP pls. with E'< 8 cngs either showed severe pericardial calcification, systolic dyslunclion, or post-radiation syndrome. Pts. with RCM showed a significantly higher E/E'-Ralio (septal MA: 264-9 vs. 124-8 cm/s; p< 0.001). Conclusion: TDI analysis of MA motion demonstrated decreased systolic and diastolic velocities in pts. with RCM and allows a differentiation between pts. with RCM and CP independent ol cardiac rhythm. The diagnostic value ol TDI analysis in CP can be limited in pts. with severe pericardial calcifications, systolic dyslunction and post-radiation syndrome.

Invited commentary

Pulsatile ventricular assist is a recognized treatment for life threatening heart failure [1Rose E.C. Gelijns A.C. Moskowitz A.J. et al.Long-term use of a left ventricular assist device for end-stage heart failure.N Engl J Med. 2001; 345: 1435-1443Crossref PubMed Scopus (3288) Google Scholar]. This type of therapy is a laborious undertaking and the complication rate following device implantation remains high, with an overall survival rate of 65% to transplant. Significant ongoing problems include bleeding, infection, right heart failure, and mechanical failure of the assist device [1Rose E.C. Gelijns A.C. Moskowitz A.J. et al.Long-term use of a left ventricular assist device for end-stage heart failure.N Engl J Med. 2001; 345: 1435-1443Crossref PubMed Scopus (3288) Google Scholar, 2Miller L.W. Patient selection for the use of ventricular assist devices as a bridge to transplantation.Ann Thorac Surg. 2003; 75: S66-71Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar]. Nonpulsatile continuous flow devices have been developed and, very recently, implanted in the hope of reducing procedural complications due to their small size, ease of implantation, and easier maintenance [3Grinda J.M. Latremouille C.H. Chevalier P. et al.Bridge to transplantation with the Debakey VAD axial pump a single center report.Eur J Cardiothorac Surg. 2002; 22: 965-970Crossref PubMed Scopus (24) Google Scholar, 4Vitali E. Lanfranconi M. Ribera E. et al.Successful experience in bridging patients to heart transplantation with the Micro- Med Debakey ventricular assist device.Ann Thorac Surg. 2003; 75: 1200-1204Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar]. Some of the potential drawbacks with these newer assist devices are the negative effects of not completely unloading the failing ventricle and the consequences nonpulsatile flow over the long term. In their paper, Klotz and colleagues attempt to address these concerns. In this small, yet well-studied series of patients, right heart catheterizations as well as echocardiograms were performed before and at an average of 3.4 months after left ventricular device implantation in a relatively similar group of patients with either a pulsatile (21 patients) or nonpulsatile device (10 patients). They found that both devices were equally effective in reducing LV pressure as measured by mean pulmonary pressure and wedge pressure. As anticipated, left ventricular volume unloading was superior in the pulsatile group and, as such, the mean arterial pressure was also higher. Interestingly, the degree of LV volume unloading in the nonpulsatile group was dependent on the length of time the device had been implanted. Device contribution to overall cardiac output was higher soon after implant and then diminished over time in a near linear fashion. Five of the ten patients with the nonpulsatile device had resumption of antegrade flow across the aortic valve and two had a return of pulsatile flow measured noninvasively. Taken together, this is consistent with an improving and remodeling ventricle overtime in the nonpulsatile group. Clinically, both groups of patients were able to exercise to at least 50 W. The overall outcome to transplant was similar in both groups, but the numbers are too small to make meaningful judgments. What this information does mean is that it is not physiologically necessary to have complete volume unloading to support the failing ventricle and the underperfused patient. Rehabilitation of both the patient and the ventricle appears possible with a nonpulsatile device, and a sign of ventricular improvement is the restoration of pulsatile flow. Whether one could further the ventricular recovery using this device to the point of explant is an intriguing concept. That being said, we need more data regarding the overall outcome and complication rate of these newer nonpulsatile devices. In those patients with profound shock where complete unloading and circulatory support is crucial, this device may not work or may require significant inotropic supplementation. Patient selection may again play a significant role in outcome.

Initial experiences with the Impella device in patients with cardiogenic shock - Impella support for cardiogenic shock.

We planned a study to assess the safety, feasibility, and efficacy of the Impella micro-axial blood pump in patients with cardiogenic shock. From January 2001 to September 2002 inclusive, 16 patients in cardiogenic shock (maximal inotropic support and with IABP in 11 cases) underwent left ventricle unloading with the Impella pump. 6 were placed via the femoral artery (patients in the coronary care unit) and 10 directly through the aorta (postcardiotomy heart failure). In three patients, the device was used in combination with ECMO. Mean age was 60 years (range 43 - 75), 11 were male. A stable pump flow of 4.24 +/- 0.28 l/min was reached (3.3 +/- 1.9 l/min in patients with ECMO and Impella). Mean blood pressure before Impella) support was 57.4 +/- 13 mmHg, which increased to 74.9 +/- 13 mmHg after 6 hours and 80.6 +/- 17 mmHg (p = 0.003) after 24 hours. Cardiac output increased from 4.1 +/- 1.3 l/min to 5.5 +/- 1.3 (p = 0.003) and 5.9 +/-1.9 l/min (p = 0.01) at 6 and 24 hours. Mean pulmonary wedge pressure decreased from 29 +/- 10 mmHg to 17 +/- 5 mmHg and 18 +/- 7 mmHg at 6 (p = 0.04) and 24 hours. Blood lactate levels decreased significantly after 6 hours of support (from 2.7 +/- 1 to 1.3 +/- 0.5 mmol/l, p = 0.004). Device-related complications included three sensor failures (no clinical action), one pump displacement (replacement) and six incidences of haemolysis (peak free plasma haemoglobin > 100 mg/dl, no clinical action). Eleven patients (68 %) were weaned, six (37 %) survived. Left ventricular unloading with the Impella pump via the transthoracic or femoral approach is feasible and safe. Support led to a decrease in pulmonary capillary wedge pressure, increase in cardiac output and mean blood pressure, and improved organ perfusion in patients with severe cardiogenic shock.

A reoperation of Adult-Type Bland-White-Garland syndrome

We present a 25-year-old female patient with Bland-White-Garland syndrome (anomalous origin of the left coronary artery from the pulmonary artery) who underwent mitral valve replacement (MVR) and coronary artery bypass grafting. She had previously undergone MVR and had been treated by the Takeuchi procedure for mitral valve regurgitation and a coronary artery anomaly, respectively, at 17 years of age. She was hospitalized with shortness of breath within 7 years of surgical intervention. Swan-Ganz catheterization revealed mild pulmonary hypertension and elevated mean pulmonary wedge pressure. Echocardiography revealed marked severe calcification of the bio valve and moderate mitral valve regurgitation. Coronary angiography revealed retrograde collateral blood flow from the right coronary artery to the left coronary artery, but intrapulmonary tunnel was not visualized by pulmonary arteriography. We performed MVR with a mechanical valve and coronary artery bypass grafting between the left internal thoracic artery and the left anterior descending artery. The postoperative course was unremarkable, and no complaints were reported during follow-up at the outpatient clinic.