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Intratumoral peak systolic velocity as a new possible predictor for detection of adnexal malignancy.

OBJECTIVE: Our purpose was to evaluate whether intratumoral blood flow velocity measured by transvaginal Doppler ultrasonography would afford better discrimination between benign and malignant adnexal tumors. STUDY DESIGN: One hundred two patients with adnexal tumors (72 benign, 30 malignant) were studied with transvaginal B-mode, color, and pulsed Doppler ultrasonography before surgery. RESULTS: Sixty-five benign tumors (90.3%) had abnormal morphologic features suggesting malignancy, and blood flow was detected in 29 (40.3%). The peak systolic velocity was 13.1 +/- 9.1 cm/sec and the resistance index was 0.563 +/- 0.177. All malignant tumors had abnormal morphologic features and blood flow was detectable in all cases. The peak systolic velocity was 23.9 +/- 11.5 cm/sec and the resistance index was 0.488 +/- 0.118. When 16 cm/sec was considered as the cutoff value of peak systolic velocity, the sensitivity and specificity of peak systolic velocity in detecting malignant adnexal tumors were 83.3% and 91.6%, respectively. The sensitivity and specificity of the resistance index (cutoff value 0.72) was 93.3% and 68.1%, respectively. There was no significant difference in sensitivity between peak systolic velocity and resistance index. The specificity of the peak systolic velocity was significantly higher than that of the resistance index (p < 0.05). Moreover, the sensitivity of the peak systolic velocity did not significantly differ from that with transvaginal ultrasonography diagnosis (86.7%), and the specificity of the peak systolic velocity was significantly higher than that of transvaginal ultrasonography (69.4%). CONCLUSION: These results suggest that peak systolic velocity obtained from intratumoral abnormal morphologic features provides a superior means for differentiating malignant from benign adnexal tumors.

Adult↗

Segmental systolic responses to brief ischemia and reperfusion in the hypertrophied canine left ventricle.

OBJECTIVES AND BACKGROUND: Left ventricular hypertrophy is associated with increased mortality, increased myocardial infarct size and an increased incidence of sudden death. Although reperfusion after ischemia has been shown to result in decreased infarct size and recovery of systolic thickening, it is unknown how left ventricular hypertrophy might influence recovery of regional systolic thickening after ischemia and reperfusion. We hypothesized that left ventricular hypertrophy might attenuate or abolish the functional response to reperfusion. METHODS: Three groups of chronically instrumented, conscious dogs (dogs with left ventricular hypertrophy and hypertension; dogs with left ventricular hypertrophy and reduced blood pressure and a control group without hypertrophy and with normal blood pressure) underwent 15 min of ischemia and 24 h of reperfusion. Segmental systolic thickening was measured by sonomicrometers and myocardial segments were grouped by percent of control segmental systolic thickening retained at 15 min of ischemia (class 1 greater than or equal to 67%, class 2 from 0% to 66%, class 3 less than 0% control systolic thickening). The recovery of each class of segment was measured serially during reperfusion. Hemodynamic variables and regional myocardial blood flow were also measured. RESULTS: There were no differences among groups in recovery of segmental systolic thickening for class 1 segments. Systolic thickening in class 2 (hypokinetic) segments was significantly depressed (p less than 0.05 compared with control value) in the group with left ventricular hypertrophy and reduced blood pressure (but not in the group with hypertrophy and hypertension) during early reperfusion; systolic thickening in class 3 (dyskinetic) segments showed a similar trend in the group with hypertrophy and reduced pressure. CONCLUSIONS: Although left ventricular hypertrophy with hypertension did not attenuate the contractile response to reperfusion, hypertrophy with reduced blood pressure was associated with significantly greater depression of segmental systolic thickening early during reperfusion.

Animals↗

Predictors of systolic and diastolic improvement in patients with dilated cardiomyopathy treated with metoprolol.

OBJECTIVES: The aim of this study was to determine which patients will have systolic and diastolic improvement after beta-blockade with metoprolol. BACKGROUND: Beta-adrenergic blocking agents improve systolic and diastolic function in patients with heart failure. However, it is unclear which patients will respond best to therapy. METHODS: We retrospectively examined baseline characteristics of 24 patients who underwent double-blind then open-label treatment with metoprolol to determine which characteristic predicted improvement in systolic and diastolic function. Degree of improvement in systolic function (22 patients) was defined by the change in left ventricular ejection fraction after 3 months of therapy. Degree of improvement in diastolic function (15 patients) was defined as the change in left ventricular end-diastolic pressure and change in the slope of the isovolumetric relaxation rate-end-systolic pressure relation. RESULTS: Both systolic blood pressure at baseline (r = 0.54, p = 0.009) and the maximal positive value of the first derivative of left ventricular pressure with respect to time (peak +dP/dt) at baseline (r = 0.39, p = 0.07) correlated with improvement in ejection fraction after metoprolol treatment. Stepwise logistic regression demonstrated that only peak systolic pressure was an independent predictor of systolic improvement. Baseline heart rate, ventricular volumes, ejection fraction and adrenergic activation, as reflected by coronary sinus norepinephrine, did not predict response. Patients with the most diastolic impairment at baseline had the most favorable diastolic improvement. Those with the lowest myocardial respiratory quotient (most fatty acid utilization) at baseline also had the most marked reduction in left ventricular end-diastolic pressure. CONCLUSIONS: These data suggest that those patients with the highest peak systolic pressure, highest left ventricular end-diastolic pressure and most prolonged isovolumetric relaxation at baseline will respond best to therapy with metoprolol. However, other patients without these characteristics may also benefit.

Adult↗

Congestive heart failure: systolic and diastolic function.

There is increasing recognition that disorders of both left ventricular systolic and diastolic function can result in congestive heart failure. As such, consideration of both the filling and emptying characteristics of the left heart is needed to evaluate the hemodynamic abnormalities present in this syndrome. Considerations of the systolic (emptying) and diastolic (filling) pumping characteristics of the left heart also provides a conceptual basis to classify and understand the pathophysiology of congestive heart failure. In this context, systolic dysfunction can be defined as impaired emptying of the LV, apparent as a decreased (< 50%) effective ejection fraction (forward stroke volume divided by end-diastolic volume). Systolic dysfunction may result from impaired myocardial contractile function, increased left ventricular afterload, and/or structural abnormalities of the left heart. Diastolic dysfunction can be defined as a condition in which filling of the LV sufficient to produce an adequate cardiac output requires an elevated pulmonary venous pressure. Thus, diastolic dysfunction is clinically manifested as pulmonary congestion. Defined in this manner, the most common cause of diastolic dysfunction is systolic dysfunction. In fact, the most common symptom of patients with systolic dysfunction is dyspnea from the resulting diastolic dysfunction. Diastolic dysfunction in the setting of normal systolic function may be due to obstruction of left ventricular filling, impaired left ventricular distensibility, or extensive external compression of the LV. Treatment of diastolic dysfunction can be accomplished by relieving myocardial ischemia, improving systolic function, lowering arterial systolic pressure, and decreasing cardiac distention.

Cardiac Output↗

Outcomes in ambulatory chronic systolic and diastolic heart failure: a propensity score analysis.

BACKGROUND: Prior studies demonstrating significant difference in outcomes in systolic and diastolic heart failure (HF) are often limited to hospitalized acute HF patients, and may be confounded by residual bias. In this analysis, we examined long-term mortality and hospitalization in a propensity score matched cohort of ambulatory chronic systolic and diastolic HF patients. METHODS: Of the 7788 patients in the Digitalis Investigation Group trial, 6800 had systolic HF (ejection fraction >45%) and 988 had diastolic HF (ejection fraction >45%). We restricted our analysis to 7617 patients without valvular heart disease: 916 diastolic HF and 6701 systolic HF. Propensity scores for diastolic HF, calculated for each patient by a non-parsimonious multivariable logistic regression model, were used to match 697 diastolic HF with 2091 systolic HF patients. Matched Cox regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for outcomes in diastolic (versus systolic) HF. RESULTS: During a median 38-month follow-up, compared with 32% mortality in systolic HF, 23% of diastolic HF patients died (HR=0.70; 95% CI=0.59-0.84; P<.0001). Respective HR (95%CI) for cardiovascular and HF mortality were 0.60 (0.48-0.74; P<.0001) and 0.56 (0.39-0.79; P=.001). All-cause hospitalizations occurred in 64% of systolic and 67% of diastolic HF patients (HR=0.99; 95% CI=0.87-1.11; P=0.801). Respective HR (95%CI) for cardiovascular and HF hospitalizations were 0.84 (0.73-0.96; P=.011) and 0.63 (0.51-0.77; P<.0001). CONCLUSIONS: Despite lower mortality and cardiovascular morbidity, diastolic HF patients had similar overall hospitalizations as in systolic HF. Ejection fraction should be assessed in all HF patients to guide therapy, with special attention to non-cardiovascular morbidity in diastolic HF.

Aged↗

Prevalence of systolic impairment in an unselected regional population with hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HC) may transition to a phase characterized by systolic impairment resembling dilated cardiomyopathy. This study retrospectively assessed the incidence of left ventricular (LV) systolic impairment at initial clinical evaluation in 248 consecutive patients with HC (mean age 53 +/- 16 years). HC with systolic impairment was diagnosed if the LV ejection fraction was <50%, calculated by echocardiography. Twenty patients (8%) had HC with LV systolic impairment at initial evaluation. Patients with systolic impairment had a greater incidence of family histories of sudden cardiac death (SCD) than patients with preserved systolic function (25% vs 5.3%, p = 0.006) and more severe functional limitations (New York Heart Association class >or=III, p <0.001). All-cause mortality and cardiovascular mortality did not differ between the 2 groups. The incidence of SCD was 1.7% in patients with normal LV ejection fractions, and no SCD was observed in patients with systolic impairment. The latter group had more frequent major cardiac events (SCD, ventricular fibrillation, aborted cardiac arrest, and first implantable cardioverter-defibrillator discharge; p = 0.03). During follow-up, 2 patients progressed to HC with systolic impairment (annual incidence 0.85%). In conclusion, systolic impairment is not exceptional in patients with HC at initial evaluation and is associated with functional deterioration and major cardiac events.

Adolescent↗

Are there sex differences in regional systolic function and wall stress in hypertrophic obstructive cardiomyopathy? A three-dimensional echocardiography study.

OBJECTIVES: Sex-related differences in left ventricular (LV) systolic function have been previously reported in patients with aortic stenosis and hypertensive heart disease. The goal of this study was to determine systolic function of the LV in male and female patients with hypertrophic obstructive cardiomyopathy and to relate it to wall thickness and wall stress, respectively. BACKGROUND: Wall thickening, a parameter of regional systolic function, is determined by wall thickness and wall stress. A comprehensive analysis of regional LV function was performed from multiplane transesophageal echocardiography with 3-dimensional reconstruction of the LV. METHODS: In 21 patients (11 men and 10 women) 4 parallel (2 basal and 2 apical) equidistant short-axis cross sections from base to apex were obtained from the reconstructed LV. In each short axis, 24 wall-thickness measurements were carried out in 15-degree intervals at end-diastole (ED) and end-systole. Thus, a total of 192 measurements were obtained in each patient. Wall thickening, a parameter of regional systolic function, was calculated as the difference of ED and end-systolic wall thickness, and fractional thickening as thickening divided by ED thickness. RESULTS: Fractional thickening and wall stress were inversely related to ED wall thickness in both men and women. Women showed better LV systolic function when compared with men (P <.001). However, when corrected for wall stress, which was lower in women, there was no sex difference in systolic function. CONCLUSIONS: There are regional differences in LV systolic function in men and women that depend on regional wall thickness and wall stress.

Cardiomyopathy, Hypertrophic↗

Reduced myocardial velocities of left ventricular long-axis contraction identify both systolic and diastolic heart failure-a comparison with brain natriuretic peptide.

BACKGROUND: Echocardiographic diagnosis of radial fractional shortening or global ejection fraction fails to diagnose all patients with heart failure; about 40%, with apparently normal global systolic function, will have elevated brain natriuretic peptide (BNP) concentrations and "pure" diastolic dysfunction. Screening methods do not include assessment of left ventricular (LV) longitudinal function, however, which is a more sensitive marker of subclinical disease. AIMS: We investigated the diagnostic potential of assessment of LV longitudinal function in suspected heart failure, in a comparison against BNP. METHODS: Fifty consecutive subjects (aged 65+/-12 years; 30 men) referred to a heart failure clinic with unexplained breathlessness were examined by echocardiography and had plasma BNP measured by fluorescence immunoassay. RESULTS: Global systolic function (ejection fraction) correlated moderately with log-transformed BNP (r=-0.54), as did global diastolic function (r=0.55 for estimated LV filling pressure, and r=-0.51 for transmitral flow propagation velocity), and radial systolic function (r=-0.60) (all p<0.001). The echocardiographic parameter that correlated best with BNP, however, was LV longitudinal systolic function (r=-0.78, p<0.001). By stepwise multiple regression analysis, BNP was predicted by longitudinal systolic velocity, in association with LV mass index and radial systolic velocity (r=0.81, r(2)=0.66, p<0.0001). The sensitivity and specificity of a longitudinal systolic velocity of </=5.5 cm/s (mean of 4 basal segments) to diagnose heart failure (defined as an elevated BNP) were 94% and 85%, respectively; the negative predictive value was 97%. CONCLUSION: Non-invasive diagnosis or exclusion of suspected heart failure, whether systolic or diastolic, can be performed accurately by echocardiographic measurement of LV longitudinal systolic function.

Aged↗

Diastolic asynchrony is more frequent than systolic asynchrony in dilated cardiomyopathy and is less improved by cardiac resynchronization therapy.

OBJECTIVES: To compare the incidence of diastolic and systolic asynchrony, assessed by tissue Doppler imaging (TDI), in patients with congestive heart failure (CHF) and severe left ventricular (LV) dysfunction, and to assess TDI changes induced by cardiac resynchronization therapy (CRT). BACKGROUND: Thirty percent of CRT candidates are nonresponders. Besides QRS width, the presence of echographic systolic asynchrony has been used to identify future responders. Little is known about diastolic asynchrony and its change after CRT. METHODS: Tissue Doppler imaging was performed in 116 CHF patients (LV ejection fraction 26 +/- 8%). Systolic and diastolic asynchrony was calculated using TDI recordings of right ventricular and LV walls. RESULTS: The CHF group consisted of 116 patients. Diastolic asynchrony was more frequent than systolic, concerning both intraventricular (58% vs. 47%; p = 0.0004) and interventricular (72 vs. 45%; p < 0.0001) asynchrony. Systolic and diastolic asynchrony were both present in 41% patients, but one-third had isolated diastolic asynchrony. Although diastolic delays increased with QRS duration, 42% patients with narrow QRS presented with diastolic asynchrony. Conversely, 27% patients with large QRS had no diastolic asynchrony. Forty-two patients underwent CRT. Incidence of systolic intraventricular asynchrony decreased from 71% to 33% after CRT (p < 0.0001), but diastolic asynchrony decreased only from 81% to 55% (p < 0.0002). Cardiac resynchronization therapy induced new diastolic asynchrony in eight patients. CONCLUSIONS: Diastolic asynchrony is weakly correlated with QRS duration, is more frequent than systolic asynchrony, and may be observed alone. Diastolic asynchrony is less improved by CRT than systolic. Persistent diastolic asynchrony may explain some cases of lack of improvement after CRT despite good systolic resynchronization.

Aged↗

Systolic and diastolic dyssynchrony in patients with diastolic heart failure and the effect of medical therapy.

OBJECTIVES: The purpose of this study was to determine the prevalence of systolic and diastolic dyssynchrony in diastolic heart failure (DHF) patients and identify the effects of medical therapy. BACKGROUND: The prevalence of systolic and diastolic dyssynchrony in DHF patients is unknown with no data on the effects of medical therapy on dyssynchrony. METHODS: Patients presenting with DHF (n = 60; 61 +/- 9 years old, 35 women) underwent echocardiographic imaging simultaneous with invasive measurements. An age-matched control group of 35 subjects and 60 patients with systolic heart failure (SHF) were included for comparison. Systolic and diastolic dyssynchrony were assessed by tissue Doppler and defined using mean and SD values in the control group. RESULTS: Systolic dyssynchrony was present in 20 patients (33%) with DHF and 24 patients (40%) with SHF and was associated in both groups with significantly worse left ventricular (LV) systolic and diastolic properties (p < 0.05 vs. control group and patients without systolic dyssynchrony). Diastolic dyssynchrony was present in 35 patients (58%) with DHF and 36 patients (60%) with SHF and had significant inverse correlations with mean wedge pressure and time constant of LV relaxation. In DHF patients, medical therapy resulted in significant shortening of diastolic time delay (39 +/- 23 ms to 28 +/- 20 ms; p = 0.02) but no significant change in systolic interval (p = 0.15). Shortening of diastolic time delay correlated well with tau shortening after therapy (r = 0.85; p < 0.001). CONCLUSIONS: Systolic dyssynchrony occurs in 33% of DHF patients, and diastolic dyssynchrony occurs in 58%. Medical therapy results in significant shortening of the diastolic intraventricular time delay which is closely related to improvement in LV relaxation.

Aged↗

Comparison of acute changes in left ventricular volume, systolic and diastolic functions, and intraventricular synchronicity after biventricular and right ventricular pacing for heart failure.

BACKGROUND: Biventricular pacing (BiV) therapy has recently been shown to improve systolic function and cause reverse remodeling in patients with advanced heart failure with electromechanical delay. In these patients, the benefit of right ventricular (RV)-based pacing was controversial. We compared the acute changes in systolic and diastolic function, left ventricular (LV) volume, and intraventricular synchronicity in BiV pacing, RV pacing, and without pacing (No) by means of echocardiography and tissue Doppler imaging (TDI). METHODS: TDI was performed in 33 patients with heart failure after undergoing pacemaker implantation, when the device was randomized to BiV, RV, and no pacing modes. RESULTS: Systolic function was only improved during BiV pacing, but not during RV pacing. This included ejection fraction (No vs RV vs BiV = 24% +/- 12% vs 25% +/- 10% vs 30% +/- 14%, P =.02 vs No), +dp/dt (P =.01), myocardial performance index (P =.01), and isovolumic contraction time (P =.03). Mitral regurgitation was only reduced during BiV pacing (P =.02). LV early diastolic function was depressed in both RV and BiV pacing, as detected by transmitral flow (97 +/- 34 vs 80 +/- 34 vs 82 +/- 32 cm/s, both P < or =.005) and TDI (mean myocardial early diastolic velocity of 6 basal segments, 3.3 +/- 1.7 vs 2.6 +/- 1.0 vs 2.6 +/- 1.0 cm/s, both P =.01). The LV end-diastolic (187 +/- 86 vs 177 +/- 84 vs 166 +/- 79, P =.003) and end-systolic (146 +/- 77 vs 138 +/- 79 vs 122 +/- 69, P =.003) volumes were only decreased during BiV pacing. For systolic synchronicity, a significant delay in peak systolic contraction in the lateral over the septal wall (171 +/- 37 vs 217 +/- 46 ms, P =.004) was revealed by TDI when there was no pacing. This was abolished by BiV pacing, in which septal contraction was delayed (195 +/- 38 vs 201 +/- 53 ms, P = not significant). However, RV pacing restored the lateral wall delay, and systolic asynchrony reappeared (190 +/- 40 vs 227 +/- 56 ms, P =.01). Diastolic asynchrony between the septal and lateral walls was not evident in these patients and was not affected by either pacing mode. CONCLUSION: Only BiV pacing, but not RV pacing, improves systolic function, and reduces mitral regurgitation and LV volumes in patients with heart failure and electromechanical delay. This is attributed to the improvement of systolic synchronicity. Diastolic synchronicity was unaffected, whereas early diastolic function could be jeopardized, by either pacing mode.

Aged↗

Severe aortic insufficiency and normal systolic function: determining regional left ventricular wall stress by finite-element analysis.

BACKGROUND: Because severe aortic insufficiency in the setting of preserved left ventricular function is often associated with a long asymptomatic period and unpredictable course on medical therapy, sensitive indices of left ventricular systolic performance are necessary for the optimal direction of therapeutic intervention. Because myocardial wall stress is closely related to both pathologic cardiac remodeling and ultimately to left ventricular decompensation, an accurate description of regional wall stress distribution may improve our ability to clinically manage these patients appropriately. The objectives of this study were (1) to define sensitive, noninvasive indices of left ventricular systolic performance to assist the clinician in the serial evaluation and early detection of increased left ventricular wall stress and, therefore, inadequate left ventricular remodeling and subsequent myocardial decompensation of patients with aortic insufficiency, and (2) to quantify differences in instantaneous global and regional end-systolic wall stress between normal subjects and patients. METHODS: Magnetic resonance imaging was performed on 23 normal volunteers and 19 patients with aortic insufficiency and normal systolic function (ejection fraction, 57% +/- 6%). Finite-element analysis was used to estimate global and regional end-systolic stress. RESULTS: End-systolic stress was significantly higher in the patient group globally (154,700 +/- 31,711 versus 96,781 +/- 23,185 dyne/cm(2); p < 0.001) and regionally (p < 0.001 in all segments) despite normal systolic function and similar end-systolic pressures. CONCLUSIONS: End-systolic stress as determined by magnetic resonance imaging and finite-element analysis may have considerable potential as a noninvasive, clinically applicable index of regional left ventricular function that may help in the serial evaluation, optimal management, and early identification of left ventricular decompensation in patients with aortic insufficiency.

Adult↗

Linear end-systolic pressure-volume relationship during pulsatile left ventricular bypass represents native heart function.

This study assessed whether the end-systolic pressure-volume relationship obtained without any interventions during pulsatile left ventricular bypass adequately represents native heart function. In 11 anesthetized Holstein calves, left ventricular pressure was measured with a micromanometer while left ventricular volume was simultaneously calculated from orthogonal left ventricular diameters measured with ultrasonic dimension transducers. End-systolic pressure and volume data were subjected to linear regression analysis to achieve an end-systolic pressure-volume relationship. Data from both caval occlusions and aortic occlusion were used for the control end-systolic pressure-volume relationship (median r = 0.941, slope = 7.4 +/- 0.8 mm Hg per milliliter per 100 gm left ventricular weight; mean +/- standard error of the mean). During left atrial-aortic bypass with a Pierce-Donachy pneumatic assist pump in the asynchronous mode, the end-systolic pressure-volume relationships were obtained without interventions to change ventricular loading conditions. During maximal ventricular unloading during full to empty pumping, termed 100%, the resulting narrow range of pressure and volume data did not yield highly linear end-systolic pressure-volume relationships (median r = 0.669, slope = 4.9 +/- 0.9 mm Hg per milliliter per 100 gm left ventricular weight). However, at reduced rates off pumping, the end-systolic pressure-volume relationships were considerably linear (80%, median r = 0.819; 60%, median r = 0.868; 40%, median r = 0.899). Slopes did not significantly differ from control values (80%, 6.9 +/- 1.1; 60%, 8.2 +/- 1.1; 40%, 7.8 +/- 1.1). The end-systolic pressure-volume relationship obtained without exogenous load changes during asynchronous, pulsatile left ventricular bypass represents native left ventricular systolic function.

Animals↗

Arterial compliance abnormalities in isolated systolic hypertension.

Arterial compliance measurements using intraarterial pulse contour analysis and a modified Windkessel model were carried out in 19 patients with isolated systolic hypertension (> or = 160/< or = 90 mm Hg) and compared to measurements in 29 patients with essential hypertension (diastolic blood pressure [BP] > or = 95 mm Hg) and 47 normotensive control subjects. Arterial capacitive compliance was significantly lower in isolated systolic hypertension than in essential hypertension (P < .0002) and significantly lower in essential hypertension than in normotensive control subjects (P < .0001). Although the isolated systolic hypertension group was older than the essential hypertension group, the reduction of capacitive compliance in isolated systolic hypertension persisted even when comparison was made with a more nearly age-matched group of essential hypertension. In contrast, oscillatory compliance was reduced similarly in isolated systolic hypertension and essential hypertension compared to normotensive control subjects (P < .0001). Although pulse pressure was greater in isolated systolic hypertension than in essential hypertension, only a weak correlation (r = -0.34) existed between pulse pressure and capacitive compliance. These data indicate that both essential hypertension and isolated systolic hypertension patients exhibit comparably abnormal structure or tone of the small vessels that are the site of oscillations or reflections in the arterial vasculature. In isolated systolic hypertension there is a profound reduction in large artery or capacitive compliance that accounts for the increase in systolic BP and decrease in diastolic BP. This abnormality cannot be accurately assessed by pulse pressure alone.

Aged↗

Pulmonary artery systolic pressures estimated by echocardiogram vs cardiac catheterization in patients awaiting lung transplantation.

BACKGROUND: At many lung transplant centers, right heart catheterization and transthoracic echocardiogram are part of the routine pre-transplant evaluation to measure pulmonary pressures. Because decisions regarding single vs bilateral lung transplant procedures and the need for cardiopulmonary bypass are often made based on pulmonary artery systolic pressures, we sought to examine the relationship between estimated and measured pulmonary artery systolic pressures using echocardiogram and catheterization, respectively. METHODS: We retrospectively reviewed all patients in our program who had measured pulmonary hypertension (n = 57). Patients with both echocardiogram-estimated and catheterization-measured pulmonary artery systolic pressures performed within 2 weeks of each other were included (n = 19). We analyzed results for correlation and linear regression in the entire group and in the patients with primary pulmonary hypertension (n = 8) and pulmonary fibrosis (n = 8). RESULTS: In patients with primary pulmonary hypertension, pulmonary artery systolic pressure was 94 +/- 27 and 95 +/- 15 mm Hg by echocardiogram and catheterization, respectively, with r(2) = 0.11; in patients with pulmonary fibrosis, 57 +/- 23 and 58 +/- 12 mm Hg with r(2) = 0.22; and in the whole group, 76 +/- 29 and 75 +/- 23 mm Hg with r(2) = 0.50. Thirty-two additional patients had mean pulmonary artery systolic pressure = 48 +/- 16 mm Hg by catheterization but either had no evidence of tricuspid regurgitation by echocardiogram (n = 22) or the pulmonary artery systolic pressure could not be measured (n = 10). CONCLUSIONS: In patients with pulmonary hypertension awaiting transplant, pulmonary artery systolic pressures estimated by echocardiogram correspond but do not serve as an accurate predictive model of pulmonary artery systolic pressures measured by catheterization. Technical limitations of the echocardiogram in this patient population often preclude estimating pulmonary artery systolic pressure.

Adult↗

Clinical criteria and biochemical markers for the detection of systolic dysfunction.

BACKGROUND: This study was designed to assess the use of clinical criteria and biochemical testing to detect systolic dysfunction. Our goal is to develop strategies that may enhance the detection and treatment of patients with early ventricular dysfunction while reducing the use of echocardiography. METHODS AND RESULTS: We compared the predictive characteristics of the plasma brain natriuretic peptide (BNP) concentration with that of a 5-point clinical score derived from elements of the history, electrocardiogram, and chest radiograph in outpatients (n = 466) referred for echocardiography because of symptoms of heart failure or risk factors for systolic dysfunction. Systolic dysfunction was defined as an ejection fraction (EF) less than 45% and was present in 10.9% of patients. By receiver operating characteristic analysis, BNP was sensitive and specific for the detection of systolic dysfunction, with an area under the receiver operating characteristic curve for the detection of EF less than 45% of 0.79. The BNP assay was abnormal in 41% of patients and identified a group with a high prevalence of systolic dysfunction (21% with an EF less than 45%), whereas a normal BNP value identified a group with a low prevalence of systolic dysfunction (4% with an EF less than 45%). The clinical score was positive in 43% of the population and identified a group with a high prevalence of systolic dysfunction (24% with an EF less than 45%). A normal score identified a group with a low prevalence of systolic dysfunction (1% with an EF less than 45%). CONCLUSION: This study supports previous studies, which showed that BNP assay predicts systolic dysfunction with acceptable sensitivity and specificity, and it underscores the effectiveness of additional readily available clinical criteria. Both of these strategies should be considered in screening for left ventricular dysfunction in populations at risk while limiting expensive cardiac imaging modalities.

Aged↗

The natural history of borderline isolated systolic hypertension.

BACKGROUND: Patients with isolated systolic hypertension are at increased risk for cardiovascular disorders. We attempted to determine whether those with borderline isolated systolic hypertension (defined as a systolic blood pressure of 140 to 159 mm Hg and a diastolic blood pressure below 90 mm Hg) have a greater risk of progression to definite (more severe) hypertension and of major morbid or fatal events than people with normal blood pressure (< 140/90 mm Hg). METHODS: A total of 2767 of the original participants in the Framingham Heart Study were monitored with biennial examinations for up to 34 years for the development of definite hypertension (defined as a systolic blood pressure of > or = 160 mm Hg, a diastolic blood pressure of > or = 90 mm Hg, or the initiation of antihypertensive therapy) and for major cardiovascular events. RESULTS: Borderline isolated systolic hypertension was the most common type of untreated hypertension among adults over the age of 60. After 20 years of follow-up, 80 percent of those with borderline isolated systolic hypertension had progression to definite hypertension, as compared with 45 percent of the normotensive participants (P < 0.001). After adjustment for age, sex, and risk factors for cardiovascular disease, participants with borderline isolated systolic hypertension had an excess long-term risk of cardiovascular disease (hazard ratio, 1.47; 95 percent confidence interval, 1.24 to 1.74) and death from cardiovascular disease (hazard ratio, 1.57; 95 percent confidence interval, 1.24 to 2.00), as compared with normotensive participants. In an analysis of pooled data from biennial examinations to study short-term sequelae, subjects with borderline isolated systolic hypertension had an increased risk of progression to definite hypertension (odds ratio, 3.84; 95 percent confidence interval, 3.35 to 4.41) and of cardiovascular disease (odds ratio, 1.39; 95 percent confidence interval, 1.06 to 1.82). CONCLUSIONS: In both the short term and the long term, subjects with borderline isolated systolic hypertension are at increased risk of progression to definite hypertension and the development of cardiovascular disease.

Adult↗

Striking effect of left ventricular systolic performance on propagation velocity of left ventricular early diastolic filling flow.

Propagation velocity of left ventricular (LV) early diastolic filling flow (PVE) has been acknowledged as a useful parameter for LV early diastolic performance; however, the effect of LV systolic performance on PVE is not fully understood. Thus the purpose of this study was to investigate such an effect. Propagation of LV early diastolic filling flow was visualized by M-mode color Doppler imaging, and the slopes of the peak velocity tracings were measured as PVE in 150 patients who underwent coronary angiography. In cardiac catheterization, mean pulmonary capillary wedge pressure, time constant tau of LV pressure decay, LV end-systolic volume index, and LV ejection fraction were obtained. In univariate regression analysis, PVE significantly correlated with LV end-systolic volume index (r = -0.68, P <.001), LV ejection fraction (r = 0.66, P <.001), and time constant tau (r = -0.52, P <.001). In multivariate regression analysis, PVE was regressed by the LV end-systolic volume index, tau, and mean pulmonary capillary wedge pressure. The contribution of each parameter to the variance of the PVE was 46%, 3%, and 2%, respectively. A break-point linear regression analysis showed that the relation between the LV end-systolic volume index and PVE was much better characterized by a broken line than a straight line. The broken line had a steeper slope in patients with LV end-systolic volume index < or =41 mL/m(2) than in those with >41 mL/m(2). These findings suggest that PVE is determined mainly by LV systolic performance and partly by both LV relaxation and LV filling pressure. Left ventricular systolic performance may play a key role in generating a much faster PVE, especially in patients with relatively better LV systolic performance.

Aged↗