Indices Of Diastolic Dysfunction Research Articles

Aortic valve sclerosis: new help from echocardiography in the assessment of cardiovascular risk

Aortic valve sclerosis: new help from echocardiography in the assessment of cardiovascular risk

Brain natriuretic peptide levels do not correlate with acute cellular rejection in De Novo orthotopic heart transplant recipients

Background The changes in brain natriuretic peptide (BNP) levels after orthotopic heart transplantation have not been previously described. The use of brain natriuretic peptide levels as a surrogate marker for cellular rejection remains controversial, with conflicting data. Methods We prospectively evaluated the potential utility of BNP levels in the first 6 months after transplantation and sought correlation with histologic grade of rejection and hemodynamic status. Results Thirty-five patients and 265 biopsy samples were included in the study. BNP levels did not correlate with histologic grade of rejection. They showed good correlation with central venous pressure and pulmonary capillary wedge pressure. BNP levels were elevated after transplant and showed a steep time-dependent decline. BNP levels correlated with echocardiographically derived indices of diastolic dysfunction. Conclusions BNP levels are not a surrogate marker for rejection in the first 2 months after orthotopic heart transplantation and do not obviate the necessity for endomyocardial biopsy. Whether BNP levels have long-term prognostic significance is unclear and remains the subject of ongoing prospective study.

Myocardial fibrosis and diastolic dysfunction in deoxycorticosterone acetate-salt hypertensive rats is ameliorated by the peroxisome proliferator-activated receptor-alpha activator fenofibrate, partly by suppressing inflammatory responses associated with the nuclear factor-kappa-b pathway

ObjectivesWe sought to clarify that a peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activator inhibits myocardial fibrosis and its resultant diastolic dysfunction in hypertensive heart disease, as well as to investigate whether inflammatory mediators through the nuclear factor (NF)-kappa-B pathway are involved in the effects. BackgroundPatients with hypertensive heart disease often have diastolic heart failure without systolic dysfunction. Meanwhile, it has been well established in atherosclerosis that PPAR-alpha activation negatively regulates early inflammation. In hypertensive hearts, however, it is still unclear whether PPAR-alpha activation inhibits inflammation and fibrosis. MethodsTwenty-one rats were randomly separated into the following three groups: deoxycorticosterone acetate (DOCA)-salt hypertensive rats treated with a PPAR-alpha activator, fenofibrate (80 mg/kg/day for 5 weeks); DOCA-salt rats treated with vehicle only; and uni-nephrectomized rats as normotensive controls. ResultsFenofibrate significantly inhibited the elevation of left ventricular end-diastolic pressure and the reduction of the magnitude of the negative maximum rate of left ventricular pressure rise and decline, corrected by left ventricular pressure (−dP/dtmax/P), which are indicators of diastolic dysfunction. Next, fenofibrate prevented myocardial fibrosis and reduced the hydroxyproline content and procollagen I and III messenger ribonucleic acid expression. Finally, inflammatory gene expression associated with NF-kappa-B (interleukin-6, cyclooxygenase-2, vascular cell adhesion molecule-1, and monocyte chemoattractant protein-1), which is upregulated in DOCA-salt rats, was significantly suppressed by fenofibrate. Activation of NF-kappa-B and expression of I-kappa-B-alpha in DOCA-salt rats were normalized by fenofibrate. ConclusionsA PPAR-alpha activator reduced myocardial fibrosis and prevented the development of diastolic dysfunction in DOCA-salt rats. The effects of a PPAR-alpha activator may be mediated partly by prevention of inflammatory mediators through the NF-kappa-B pathway. These results suggest that treatment with PPAR-alpha activators will improve diastolic dysfunction in hypertensive heart disease.

Elafin-overexpressing mice have improved cardiac function after myocardial infarction.

Elevated serine elastase activity after myocardial infarction can contribute to remodeling associated with left ventricular dilatation and dysfunction. We therefore assessed the effects of overexpressing the selective serine elastase inhibitor elafin in transgenic mice in which a myocardial infarction was caused by ligation of the left anterior descending coronary artery (LAD). Elevated serine elastase activity was observed in nontransgenic littermates as early as 6 h after LAD ligation and persisted at 4 and 7 days but not in sham-operated or elafin-overexpressing transgenic mice. Myeloperoxidase activity (index of inflammatory cells) and matrix metalloproteinase 2 were also increased but only at 4 and 7 days and only in nontransgenic mice (P < 0.05 for both comparisons), and this increase correlated with inflammatory cell infiltration. Echocardiographic study at 4 days revealed indexes of diastolic dysfunction in nontransgenic versus elafin-overexpressing mice (P < 0.05). Morphometric and biochemical analyses at 28 days indicated impairment in cardiac performance, with greater scar thinning and infarct expansion in nontransgenic versus elafin transgenic littermates (P < 0.05 for all comparisons). Thus serine elastase inhibition appears to suppress inflammation, cardiac dilatation, and dysfunction after myocardial infarct.

Doppler-echocardiographic indices of diastolic function in heart failure admissions with preserved left ventricular systolic function.

Many patients admitted to hospital with heart failure have preserved left ventricular (LV) systolic function. The incidence of isolated diastolic dysfunction as a cause of such admission remains unclear. We aimed to examine diastolic function in unselected admissions from the community with heart failure using the European Study Group on Diastolic Heart Failure (ESGDHF) Doppler-echocardiographic indices of diastolic dysfunction. Primary heart failure was confirmed in 210 of 309 sequential admissions with suspected heart failure. Doppler echocardiography was used to assess left ventricular ejection fraction, wall thickness and parameters of diastolic function including E:A ratio, E-wave deceleration time and isovolumic relaxation time. Of 210 patients studied (118 female), ejection fraction was <45% in 111, leaving a population of 99 with preserved systolic function. We excluded those with significant valvular disease, leaving 56 patients (mean age=77 years) with an ejection fraction >45% and no other relevant abnormality. Twenty were in atrial fibrillation. E-wave deceleration time was >280 ms in 42%. E:A was reversed in 30 of 36 patients in sinus rhythm, but only seven met the ESGDHF criterion of E:A<0.5. Isovolumic relaxation time was >105 ms in 38%. Wall thickness was increased in 75% of cases. The ESGDHF Doppler-echocardiographic criteria for diastolic heart failure were fulfilled in 43%. In clinically confirmed heart failure, 27% of patients had preserved systolic function and no significant valvular disease. Only 43% of this group had confirmed diastolic heart failure by these ESGDHF criteria. The pathophysiological basis of the syndrome in the remaining 57% remains unclear.

Ambulatory blood pressure monitoring: technique and application in the study of cardiac dysfunction and congestive heart failure.

Ambulatory blood pressure monitoring has become a widely used method of blood pressure and heart rate evaluation in the free-living subject. Recently, ambulatory monitoring has become covered by Medicare for the evaluation of "white-coat" hypertension. Although the technique provides only intermittent readings throughout the 24-hour period, average blood pressures obtained in this way correlate well with a variety of hypertensive disease processes and are also a better prognostic marker for future cardiovascular events than office blood pressure. Ambulatory blood pressure averages also correlate well with indices of diastolic dysfunction. In patients with congestive cardiac failure and systolic dysfunction, ambulatory monitoring suggests an impaired circadian blood pressure profile with high nocturnal blood pressure. Further research is needed on the relationship between ambulatory blood pressure and cardiac dysfunction, as well as the impact of observed circadian blood pressure changes on outcome. (c)2001 CHF, Inc.

Propagation velocity: an indicator of diastolic dysfunction during coronary revascularization surgery

Ti, L.; Djaiani, G.; Podgoreanu, M.; Mackensen, B.; McCreath, B.; Bainbridge, D.; Albahrani, M.; Ellingham, J.; Swaminathan, M.; Mathew, J. Author Information

Preconditioning during percutaneous transluminal coronary angioplasty by endogenous and exogenous adenosine

Background The purpose of this study was to assess whether pharmacologic preconditioning by exogenous or endogenous adenosine prevents the deterioration of hemodynamic function and left ventricular performance during percutaneous transluminal coronary angioplasty (PTCA). Ischemic preconditioning renders the heart more resistant to subsequent ischemia. Adenosine plays a key role in its pathogenesis. Coronary angioplasty is a suitable model for the induction of myocardial ischemia. Methods and Results We investigated 30 patients receiving PTCA of the left anterior descending coronary. Patients were randomly allocated to either dipyridamole, leading to the liberation of endogenous adenosine (0.5 mg/kg body weight, intracoronary), exogenous adenosine (20 mg intracoronary), or an equal amount of saline. Chest pain, tolerated inflation time, and ST-segment shift were registered. Left ventricular hemodynamics, isovolumetric phase indexes, indexes of volume, ejection fraction, and indexes of diastolic dysfunction were analyzed. Patients receiving endogenous or exogenous adenosine tolerated longer balloon inflation times (dipyridamole, 208 ± 23 seconds; adenosine, 188 ± 41 seconds; control, 153 ± 36 seconds; P <.05). Deterioration of left ventricular ejection fraction was less severe after adenosine (72% ± 5% before PTCA vs 64% ± 6% during angioplasty; P =.11) and could be prevented by intracoronary dipyridamole (69% ± 12% before PTCA vs 68% ± 11% after PTCA; P <.01) compared with the control group (71% ± 7% before PTCA vs 60% ± 7% during angioplasty). Conclusions Intracoronary application of exogenous adenosine and liberation of endogenous adenosine increase the tolerance to ischemia and prevent deterioration of left ventricular function during ischemia. These findings can be attributed to ischemic preconditioning. However, endogenous adenosine exceeds the protective effects of exogenous adenosine. (Am Heart J 2000;140:813-20.)

Diastolic dysfunction and heart failure: causes and treatment options.

Diastolic dysfunction is the underlying problem in one third of patients with heart failure, but it is still not well understood. Carefully excluding other causes of heart failure and recognizing indicators of diastolic dysfunction on invasive and noninvasive tests are important in establishing the diagnosis and in guiding therapy. Left ventricular relaxation and stiffness and left atrial function are the most important factors acting together to maintain adequate cardiac output under normal filling pressure. Echocardiography is the most important tool for the diagnosis of diastolic heart dysfunction. It is portable, safe, and excludes other causes of heart failure, such as valvular disease. Diuretics can be used to reduce volume overload, but caution is advised, as aggressive diuresis decreases stroke volume more in diastolic dysfunction than in systolic dysfunction.

Prevalence of Sleep-Disordered Breathing in Diastolic Heart Failure

Sleep-disordered breathing (SDB) is common in congestive heart failure. While isolated diastolic heart failure (DHF) accounts for up to a third of all cases of congestive heart failure, the prevalence of SDB in DHF is unknown. We aim to determine the prevalence and characteristics of SDB in a group of patients with symptomatic DHF. Twenty subjects with symptomatic DHF (New York Heart Association class II or III) and isolated diastolic dysfunction on echocardiography were assessed with lung function tests, modified sleep and health questionnaire, and overnight polysomnography. Significant SDB was defined as an apnea/hypopnea index (AHI) > 10. Thirteen female and seven male subjects (mean age, 65+/-6.0 years; mean body mass index (BMI), 28+/-3.2) were evaluated, of whom 17 (85%) had a diagnosis of hypertension. Overall sleep quality was poor, with fragmentation and frequent arousals associated with respiratory events. Fifty-five percent of the patients had significant SDB, mainly obstructive apneas. BMI and the prevalence of hypertension were similar in patients with and without SDB. The deceleration time, an index of diastolic dysfunction, was more prolonged in the group with SDB (236+/-40 ms vs 282+/-31 ms; p<0.05). As a group, a lower minimum percentage arterial oxygen saturation during sleep, but not the AHI was associated with more severe degree of diastolic dysfunction on echocardiogram, including a lower ratio between the early peak transmittal flow velocity and the late peak atrial systolic velocity (rho=0.57; p<0.05) and a prolonged isovolumic relaxation time (rho=-0.54; p<0.05). SDB is common in patients with DHF. Patients with DHF and SDB may be associated with worse diastolic dysfunction than those without SDB, although a causal relationship remains to be established.

Successful radiofrequency catheter ablation of automatic atrial tachycardia with regression of the cardiomyopathy picture.

Ectopic atrial tachycardia (EAT) is often refractory to pharmacological suppression, and if uncontrolled, it can lead to cardiomyopathy. Although RF current catheter ablation therapy has been effective in eliminating the arrhythmia, there is limited information, particularly in adult patients with regard to the reversal of the tachycardia induced cardiomyopathy. Four adult patients, 20-56 years of age, and a 6-year-old boy, were referred with refractory EAT. Four patients had heart failure and three had depressed LV function by echocardiographic criteria. All patients underwent electrophysiological study, and RF ablation was successful in abolishing the arrhythmogenic foci. Of these, four were located in the right atrium and one in the left atrium, and were identified by recording of the earliest atrial activation. No complications occurred. Termination of the EAT resulted in symptomatic improvement. Serial echocardiographic assessment of LV function indicated a significant reversal of the cardiomyopathy picture with reduction in chamber size and recovery in systolic function; indices of diastolic dysfunction persisted in one patient. Chronic, uncontrolled EAT can cause tachycardia induced cardiomyopathy. The picture of the cardiomyopathy resolves after elimination of the focus. RF ablation is both effective and safe, and may be considered as early therapy, particularly in patients with incessant EAT and ventricular dysfunction.

Effects of venous return reduction in hypertensive patients: Is there a Doppler diastolic dysfunction index independent of preload reduction?

The aim of this study was to evaluate the effects of preload reduction on the Doppler transmitral flow pattern in the presence of diastolic dysfunction (hypertensive patients) and normal diastolic function (normal subjects) to identify, if present, one or more indexes of abnormal diastolic ventricular filling independent of variations in preload. For this purpose Doppler echocardiography was performed in 17 patients with hypertension and in 18 normal subjects under basal conditions and after 5 minutes of blood pressure cuff inflation at the root of the four limbs. The two groups showed a similar response to preload reduction: a significant reduction in peak velocity and the time-velocity integral of the E wave and in the ratio of peak velocities of E and A waves. Therefore the differences in left ventricular filling patterns between hypertensive and normal subjects observed under basal conditions were still present after preload reduction. The comparison between normal subjects after preload reduction and hypertensive patients in the basal state showed a higher peak velocity and time-velocity integral of the A wave in the latter (61.2 ± 16.2 vs 46.2 ± 9 cm/sec [ p < 0.002] and 5.4 ± 1.8 vs 3.7 ± 1 cm [ p < 0.002], respectively) with no differences in the ratios of peak velocities and time-velocity integrals of the E and A waves. It was concluded that the response of the Doppler transmitral flow pattern to preload reduction appears to be similar in normal subjects and patients with hypertension, irrespective of the presence of diastolic dysfunction, and the peak velocity and time-velocity integral of the A wave may be considered indexes of diastolic dysfunction independent of preload reduction.

Normalization of Doppler indices of diastolic dysfunction during pacing is a sign of ischemic mitral regurgitation

Twenty-three patients with angina who were undergoing diagnostic cardiac catheterization underwent cardiac pacing with simultaneous hemodynamic and Doppler echocardiographic evaluation to assess the effects of pacing-induced ischemia on mitral valve inflow velocity. Seventeen patients had significant coronary artery disease, and six patients had normal coronary arteries. Doppler and hemodynamic measurements were performed at rest and immediately after pacing was discontinued to 91% ± 7% of maximal predicted heart rate. Seven patients experienced new or significant increases in severity of mitral regurgitation after pacing as revealed by Doppler examination. This group had a significant increase (p = 0.007) in early but not in late peak filling velocities immediately after pacing was discontinued, with a resultant decrease in late to early ratios, which decreased from 1.01% ± 0.12 to 0.70% ± 0.19 (p = 0.006). Left ventricular end-diastolic pressure increased significantly from 16.7% ± 6.8 mm Hg to 29.4% ± 5.3 mm Hg after cardiac pacing (p < 0.001). Patients with coronary disease who did not develop mitral regurgitation also had significant increases in left ventricular end-diastolic pressure from 18.7% ± 5.8 mm Hg to 24.3% ± 8.6 mm Hg (p < 0.05). There were no changes in late or early wave amplitude, late to early ratio, or other Doppler measurements in any of the other groups. We conclude that mitral regurgitation caused by pacing-induced myocardial ischemia normalized Doppler indices of mitral inflow, which in turn, may mask persistent or worsened left ventricular diastolic dysfunction.