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PubMed1986

Ventricular systolic and diastolic impairment during pacing-induced myocardial ischemia in coronary artery disease: simultaneous hemodynamic, electrocardiographic, and radionuclide angiographic evaluation.

This study examined the impairment in systolic and diastolic performance of both ventricles during pacing-induced myocardial ischemia in 12 men with coronary artery disease. Simultaneous hemodynamic, ECG, and radionuclide angiographic assessments were made: pre pacing (pre-P); intermediate pacing (P-1); maximum pacing (P-2); and immediately after pacing (post pacing (P-P). The prepacing measurements were made with the patient in the supine position and during leg elevation. Pacing produced a leftward and upward shift in the diastolic pressure-volume relation, a progressive decrease in left ventricular (LV) end-diastolic volume (p less than 0.003) and right ventricular (RV) end-diastolic volume (p less than 0.01), concomitant with an increase in the pulmonary artery wedge pressure (p less than 0.004) and the right atrial pressure (p less than 0.04). The shift in the LV pressure-volume relation was associated with an initial increase (P-1), followed by a decrease (P-2) in the peak filling rate (p less than 0.001). Pacing also resulted in systolic dysfunction: abnormal LV ejection fraction responses in eight patients, LV regional wall motion abnormalities in eight patients, and abnormal RV ejection fraction responses in seven patients. Leg elevation resulted in a 7% increase in cardiac output, a 20% increase in RV end-diastolic volume, a 28% increase in right atrial pressure, a 29% increase in pulmonary artery wedge pressure, and a 10% increase in LV end-diastolic volume (p less than 0.05). Thus, the ischemic response to pacing results in systolic and diastolic LV and RV dysfunction, with the diastolic impairment being more frequent than the systolic impairment.

Aged↗
PubMed1990

Does intracoronary infusion of Fluosol-DA 20% prevent left ventricular diastolic dysfunction during coronary balloon angioplasty?

Distal intracoronary infusion of the perfluorochemical Fluosol-DA 20% has been shown to prevent systolic dysfunction during coronary artery balloon occlusion in coronary angioplasty. To assess its effect on global diastolic dysfunction, a randomized, single-blind, crossover protocol comparing intracoronary infusion of Fluosol or no infusion (control) was performed during 60 s balloon inflations in 10 patients (mean age 67 years) undergoing coronary angioplasty. Assessment of global systolic and diastolic function was obtained with high fidelity micromanometer measurements of left ventricular pressure. Eighteen pairs of balloon inflations (Fluosol versus control) were analyzed. Patients reported significantly less severe chest pain during inflations accompanied by Fluosol compared with control. However, during coronary balloon occlusion, no significant differences in the changes from baseline values were observed between Fluosol and control with regard to ventricular relaxation, including the time constant of early ventricular relaxation (tau) and maximal rate of fall in left ventricular pressure (maximal negative dP/dt). No differences between Fluosol and control were observed in terms of the increase in end-diastolic pressure or minimal diastolic pressure during balloon inflation. Mean systolic pressure decrease from baseline values was greater during control than during Fluosol inflations (-9.0 +/- 3.3 mm Hg, p = 0.013), but no significant difference was observed in the change in maximal rate of rise in left ventricular pressure (maximal positive dP/dt). These results suggest that Fluosol does not preserve global left ventricular diastolic function during coronary balloon occlusion, possibly because of its limited oxygen delivery capability relative to arterial blood.

Aged↗
PubMed2003

Assessment of regional systolic and diastolic dysfunction in familial hypertrophic cardiomyopathy using MR tagging.

Diastolic and systolic left ventricular (LV) dysfunction often significantly contribute to disabling symptoms in familial hypertrophic cardiomyopathy (FHC). This study compares regional LV function (midwall circumferential strain) during systole and diastole in eight FHC patients and six normal volunteers (NVs) using MR tagging. A prospectively-gated fast gradient-echo sequence with an echo-train readout was modified to support complementary spatial modulation of magnetization (CSPAMM) tagging and full cardiac cycle data acquisition using the cardiac phase to order reconstruction (CAPTOR), thus providing tag persistence and data acquisition during the entire cardiac cycle. Total systolic strains in FHC patients were significantly reduced in septal and inferior regions (both P < 0.01). Early-diastolic strain rates were reduced in all regions of the FHC group (all P < 0.03). The combination of CSPAMM and CAPTOR allows regional indices of myocardial function to be quantified throughout the cardiac cycle. This technique reveals regional differences in systolic and diastolic impairment in FHC patients.

Cardiomyopathy, Hypertrophic↗
PubMed2000

[Use of tissue Doppler echocardiography].

Tissue Doppler Echocardiography (TDE) is a new noninvasive technique which shows myocardial tissue by color-mapping. It's based on the color Doppler and used to assess in a direct way left ventricular systolic and diastolic function. It helps to measure velocities, acceleration and energy signal within the myocardial wall. The transmural gradient of velocities can be calculated too. TDE can be used to detect regional systolic dysfunction due to myocardial ischemia and viable myocardium. It gives specific view of intracardiac structures and is useful for identification tumors, thrombus and vegetations.

Blood Flow Velocity↗
PubMed1987

Echocardiographic features of idiopathic hemochromatosis.

To characterize cardiac involvement in idiopathic hemochromatosis, clinical records and 2-dimensional (2-D) echocardiograms of 24 patients with idiopathic hemochromatosis were reviewed. The 17 men and 7 women were 24 to 80 years old (mean 48). Of 19 patients without valvular, ischemic, hypertensive or other known heart disease, 7 (37%) had structural and functional echocardiographic abnormalities attributed to idiopathic hemochromatosis (group 1) and 12 had normal echocardiographic findings (group 2). Age, gender and laboratory markers of iron overload did not differentiate patients with cardiac dysfunction (group 1) from those without cardiac dysfunction (group 2). In group 1, echocardiographic abnormalities included chamber dilatation and global systolic dysfunction. Increased wall thickness was not a feature of idiopathic hemochromatosis. All group 1 patients had abnormal electrocardiographic findings and cardiomegaly on radiography. Despite therapeutic phlebotomy, 4 patients in this group died, between 0.5 and 30 months after echocardiography, because of congestive heart failure. In conclusion, there is a spectrum of cardiac dysfunction in idiopathic hemochromatosis. In patients with idiopathic hemochromatosis and left ventricular dysfunction, absolute wall thickness is normal. Survival is poor in patients with idiopathic hemochromatosis and severe left ventricular dysfunction.

Adult↗
PubMed1985

Treatment of hypertrophic cardiomyopathy: relation to pathological mechanisms.

In patients with hypertrophic cardiomyopathy, clinical symptoms such as exertional dyspnea, angina and collapse are considered to be rather the consequence of diastolic than of systolic dysfunction of the left ventricle. Beta-blocker therapy is aimed at reducing systolic overcontraction while calcium blockers predominantly therapy is aimed at reducing systolic overcontraction while calcium blockers predominantly improve diastolic filling characteristics. Therefore 61 consecutive patients with well defined hypertrophic cardiomyopathy were treated with calcium channel blockers: 60 patients with verapamil at average dose 530 mg (320 to 720 mg/d) and one patient received 30 mg nifedipine. All patients had clinical, noninvasive and cardiac catheterization evaluation at the time of entry into the study. Therapy was continued for an average of 54 months (10 to 96). Follow-up studies were performed at 6-month intervals. Subjective improvement was achieved in 47 of 55 symptomatic patients (85%). Heart size, judged as heart volume from tele-chest X-ray in supine position, showed a reduction in 36/61, no change in 15/61 and increase in 10/61. On average in all 61 patients, a significant reduction from 947 to 833 ml/1.73 m2 was seen. Twenty-six patients who had been followed for an average of 24 months prior to verapamil therapy on beta blockers or no treatment had heart volume increases averaging 12% in the pre-verapamil period. Electrocardiography (ECG) showed a significant reduction in QRS amplitude and a tendency towards normalization of ST/T segments. Serial echocardiography study showed small but significant reduction in left atrial diameter. Repeat catheterization was performed in 19 patients and a significant reduction in intraventricular pressure gradient, left ventricular muscle mass and coronary artery diameter was demonstrated. Three patients died during the study (256 patient-treatment-years) for an annual mortality rate of 1.3%. This mortality is considerably lower than reported for patients receiving no treatment, beta-blockade, or surgery. Of all 61 patients only one had surgery related to the hypertrophic cardiomyopathy. One patient had the dose of verapamil reduced because of the occurrence of heart block. No patient discontinued the drug because of side-effects. Utilizing serial noninvasive and invasive studies, we conclude that verapamil therapy in hypertrophic cardiomyopathy results in objective and subjective improvement, a low death rate and little need for operation as compared to standard therapy.

Adolescent↗
PubMed1999

Candesartan in heart failure--assessment of reduction in mortality and morbidity (CHARM): rationale and design. Charm-Programme Investigators.

BACKGROUND: Chronic heart failure (CHF) is an increasing burden to health care. Pharmacological treatment with angiotensin-converting enzyme (ACE) inhibitors and beta blockers improve survival and reduce hospitalizations in patients with low left ventricular ejection fraction (LVEF). Despite these therapies, morbidity and mortality remains problematic. Furthermore, 30% to 50% of patients with CHF have a preserved LVEF. It is not known if treatments are of benefit in this group. DESIGN: Candesartan in Heart Failure-Assessment of Reduction in Mortality and Morbidity (CHARM) is a program designed to investigate the clinical usefulness of the long-acting angiotensin II type 1 receptor blocker, candesartan cilexetil, in a broad spectrum of patients with symptomatic heart failure. Patients with systolic dysfunction, tolerant or intolerant to an ACE-inhibitor, and patients with preserved systolic function are included. Specifically, the CHARM program consists of 3 independent, parallel, placebo-controlled studies in patients with (1) LVEF less than or equal to 40%, ACE-inhibitor treated (n = 2,300); (2) LVEF less than or equal to 40%, ACE-inhibitor intolerant (n = 1,700); (3) LVEF greater than 40%, not treated with ACE inhibitors (n = 2,500). The 3 studies will be combined to evaluate the effect of candesartan cilexetil on all-cause mortality in the broad spectrum of symptomatic heart failure. The primary objective in each trial is to evaluate the effects on the combined endpoint of cardiovascular mortality or CHF hospitalization. Other endpoints include the effects on myocardial infarction, all-cause hospitalization, and resource utilization. CHARM is intended to randomize 6,500 patients with symptomatic heart failure from 26 countries in Europe, the United States, Canada, South Africa, and Australia. The CHARM program started to enroll patients in March 1999. The follow-up period is a minimum of 2 years. The study is expected to end in the third quarter of 2002.

Adolescent↗
PubMed2005

Calcium antagonists: effects on cardio-renal risk in hypertensive patients.

Calcium antagonists comprise 2 main subclasses, dihydropyridines and nondihydropyridines, and have been studied extensively in hypertensive patients. Early meta-analyses suggested that short-acting calcium antagonists were associated with higher mortality rates resulting from cardiovascular events and other etiologies. Recent meta-analyses failed to show any substantive difference between long acting calcium antagonists and other antihypertensive drug classes with regard to cardiovascular outcomes in those with low to moderate cardiovascular risk or kidney disease progression among those with stage 2 or 3 nonproteinuric kidney diseases. The data from calcium antagonist trials are consistent in that they decrease stroke incidence but fail to protect against new-onset heart failure. In people with proteinuric kidney disease, that is > 300 mg protein/gram creatinine, use of dihydropyridine calcium antagonists to lower blood pressure without the use of agents that block the renin angiotensin aldosterone system does not provide optimal slowing of nephropathy progression. This relates directly to lack of antiproteinuric effects with this subclass and not seen with nondihydropyridine agents that reduce proteinuria to a greater degree than dihydropyridines. Thus, calcium antagonists are safe and as efficacious as other antihypertensive agents to reduce cardiovascular risk. They should be avoided in people with systolic dysfunction but may be used for blood pressure lowering in people with preserved systolic function. Dihydropyridine calcium antagonists should only be used in conjunction with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers in proteinuric kidney disease because they will not optimally slow kidney function loss in their absence.

Calcium Channel Blockers↗
PubMed2005

Heart involvement and systemic sclerosis.

Scleroderma heart involvement (SHI) is often manifest, and virtually always present when accurately searched and holds a significant prognostic value. Myocardial involvement by patchy fibrosis (secondary to both repeated ischaemia and immunoinflammatory damage) leads to ventricular diastolic dysfunction, whereas right ventricle overload and failure may complicate pulmonary hypertension. Left ventricular systolic dysfunction is present in a minority of patients, namely those presenting atherosclerotic coronary artery disease and/or arterial hypertension, sometimes triggered by sclerodermic renal involvement. Dysrhythmias and conduction disturbances are considered an hallmark of SHI, facilitated by autonomic dysfunction. SHI is frequently linked to parenchimal and/or vascular lung disease; they determine symptom occurrence, particularly dyspnoea, fatigue, palpitations and chest pain when pericardium is affected. Accurate cardiologic baseline screening and subsequent follow-up are mandatory in all patients, initially consisting in some noninvasive diagnostic procedures: visit, electrocardiogram (EKG), chest X-ray, Doppler-echocardiography. When needed, these examinations should be integrated by EKG Holter-monitoring, cardiopulmonary stress tests, cardiac magnetic resonance imaging, nuclear studies of myocardial function and perfusion, cardiac catheterization to better estimate pulmonary hypertension, and cardiac natriuretic hormone evaluation. Several vasodilator approaches (prostacycline or NO/endothelin) may counteract the microvascular dysfunction at peripheral and cardiopulmonary level, and fight the sequelae of pulmonary hypertension.

Fibrosis↗
PubMed1995

Postburn cardiac contractile function and biochemical markers of postburn cardiac injury.

BACKGROUND: In vivo assessment of cardiac injury and contractile deficits after thermal injury remain difficult as neurohumoral compensatory mechanisms maintain cardiac output. While measurement of creatine kinase (CK) and the isoenzyme of creatine kinase (CKMB) have been used as clinical indicators of cardiac injury, these biochemical markers are not completely specific for cardiac muscle. Cardiac protein troponin I (cTnI) is unique to the myocardium but can be detected in the systemic circulation within three to four hours after cardiac injury. The purpose of this study was to examine cardiac contractile function at several postburn intervals and to correlate the appearance of cardiac dysfunction with biochemical measures of cardiac injury (serum concentration of CK, CKMB, and cTnI). STUDY DESIGN: New Zealand white rabbits were deeply anesthetized and a scald burn comprising 34 percent of the total body surface area (n = 36) or sham burn (n = 36) was accomplished using a template device. All burn rabbits were given lactated Ringer's solution (4 mL/kg/percent burn, Parkland formula). Blood samples were collected immediately prior to sacrifice in six animals from both burn and control groups, and animals were sacrificed either two, four, six or 24 hours after burn. Cardiac function was assessed in left ventricular preparations (Langendorff) and serum CK, CKMB, and cTnI levels were determined. RESULTS: Cardiac dysfunction occurred at all times after burn as indicated by a lower peak systolic left ventricular pressure and +/- dP/dt maximum compared with time-matched shams and the shift of left ventricular function curves plotted for burn groups downward and to the right of those calculated for shams, p < 0.05. Left ventricular systolic dysfunction after burn correlated with a progressive rise in cTnI and CK but not CKMB. CONCLUSIONS: The cardiospecificity of the cTnI eliminates concerns about tissue source associated with CK and CKMB and provides a biochemical measure of cardiac injury that is consistent with in vitro assessment of cardiac dysfunction.

Animals↗
PubMed2006

Atrial and ventricular echocardiographic correlates of the extent of pulmonary embolism in the elderly.

BACKGROUND: Acute pulmonary thromboembolism (PTE) can be associated with right ventricular (RV) dysfunction. The relative importance of individual echocardiographic parameters, including those suggesting interdependence between right and left heart chambers, in predicting thromboembolic burden in elderly patients with acute PTE is unknown. METHODS: We retrospectively studied the transthoracic echocardiograms of 63 elderly patients (age 71 +/- 16 years) with acute PTE, and assessed which individual echocardiographic parameters identified more than 30% pulmonary artery obstruction on the basis of quantitative ventilation/perfusion pulmonary scintigraphy. RESULTS: RV hypokinesis (visual grade 0-3, P = .02), and the quantitative parameters RV end-systolic area (P = .005) and RV ejection area (P = .01) were associated with more extensive pulmonary artery obstruction. Although right atrial end-systolic area and RV end-diastolic area did not correlate with extent of PTE, the ratio of RV:left ventricular end-diastolic area (P = .003), and ratio of right:left atrial end-systolic area (P = .004), were strongly associated with the extent of pulmonary artery obstruction. These transthoracic echocardiographic parameters were independent of clinical variables such as prior chronic lung disease, congestive cardiac failure, or prior PTE. CONCLUSION: RV systolic dysfunction, RV end-systolic dilatation, right:left atrial end-systolic area ratio, and RV:left ventricular end-diastolic area ratio correlate with extent of PTE in the elderly.

Aged↗
PubMed2005

Prognostic significance of time-delay to peak creatine kinase after direct percutaneous coronary intervention in acute myocardial infarction patients.

The aim of the present study was to investigate the prognostic significance of time-delay to peak creatine kinase (CK) after successful direct percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). Our 240 consecutive first AMI attack subjects admitted within 5 hours from onset were successfully reperfused by direct PCI therapy. Subjects were divided into two groups according to the upper quartile value of peak-CK time from onset, the early peak-CK group (peak-CK time < or = 16 hours from onset, n = 180) and the late peak-CK group (peak-CK time > 16 hours, n = 60). (I) The early ST-segment resolution rate was lower in the late peak-CK group compared with the early peak-CK group (P < 0.05), and there were significantly fewer patients with preinfarction angina pectoris in the late peak-CK group than in the early peak-CK group (P < 0.01). (II) LVEF in the chronic stage was significantly lower in the late peak-CK group than in the early peak-CK group (49 +/- 13% versus 57 +/- 13%, P < 0.001). (III) There were significantly more patients with major complications in the late peak-CK group than in the early peak-CK group (required CABG: 10% versus 3%, P < 0.05; cardiac death: 18% versus 3%, P = 0.0001). (IV) Multivariate analysis identified late peak-CK as an independent predictor of cardiac death (Odds ratio 7.91, 95% C.I. 1.40-44.11, P < 0.05). In patients with AMI, the time-delay to peak-CK after successful direct PCI may be closely related to left-ventricular systolic dysfunction and poor patient outcome, including mortality.

Adult↗
PubMed2002

Usefulness of pulsed tissue Doppler imaging for evaluating systolic and diastolic left ventricular function in patients with AL (primary) amyloidosis.

To clarify whether pulsed tissue Doppler imaging at multiple left ventricular LV sites could help to explain the mechanism of congestive heart failure (CHF) in patients with primary amyloidosis, we examined 86 consecutive patients with primary amyloidosis confirmed by biopsy (group I, 31 patients without cardiac involvement; group II, 31 patients with evidence of heart involvement but no CHF; and group III, 24 patients with heart involvement, clinical CHF, and normal fractional shortening >28%). Peak early diastolic myocardial velocities in group II were significantly lower than those in group I, and the values in group III were also significantly lower than those in group II at most sites. In contrast to diastolic abnormalities, peak systolic wall motion velocities in group III were significantly lower than those in group II, but there were no significant differences between groups I and II. Thus, cardiac amyloidosis is characterized by an initial impairment in early cardiac relaxation, whereas CHF is associated with an impairment of peak systolic wall motion velocities, most prominently seen in the longitudinal axis. This systolic dysfunction can be detected by pulsed tissue Doppler imaging, even when ejection fraction is in the normal range.

Amyloidosis↗
PubMed2005

Cardiac function in borderline hypothyroidism: a study by pulsed wave tissue Doppler imaging.

OBJECTIVE: In subclinical hypothyroidism (SH), impaired diastolic function has been documented at rest and on effort, while systolic dysfunction has only been assessed on effort. DESIGN: The aim of the present study was: (a) to further assess systolic function at rest in SH; and (b) to ascertain whether cardiac dysfunction could precede TSH increase in euthyroid patients with a high risk of developing SH. METHODS: We studied 32 patients with classical Hashimoto's thyroiditis (22 with increased serum TSH (> 3 mU/ml - group A), and 10 with normal serum TSH (< 3 mU/ml - group B)); a third group (C), which included 13 healthy controls. All subjects underwent pulsed wave tissue Doppler imaging (PWTDI) to accurately quantify the global and regional left ventricular function. RESULTS: When compared with group C, PWTDI indices showed that in both groups A and B there was a significant impairment of systolic ejection (P < 0.001 and P < 0.05, respectively), a delay in diastolic relaxation (P < 0.001 and P < 0.05, respectively) and a decrease in the compliance to the ventricular filling (P < 0.05). Several significant correlations were found between PWTDI parameters and serum-free T(3) and T(4) and TSH concentrations. CONCLUSION: PWTDI is a sensitive technique that allows detection of both diastolic and systolic abnormalities, not only in patients with SH, but also in euthyroid subjects with a high risk of developing thyroid failure. Futhermore, the significant correlations of several PWTDI indices with serum FT(3) and TSH concentrations strongly support the concept of a continuum spectrum of a slight thyroid failure in autoimmune thyroiditis extending to subjects with serum TSH still within the normal range.

Adult↗
PubMed2006

Detection of preclinical left ventricular dysfunction in Fabry disease: the contribution of tissue Doppler.

INTRODUCTION: Fabry disease is a rare X-linked lysosomal storage disorder caused by a deficiency of alpha-galactosidase, which results in progressive intracellular accumulation of glycosphingolipids in various tissues. Cardiac involvement is frequent, with left ventricular (LV) hypertrophy (concentric, apical or asymmetric septal) as the most common finding. Evaluating LV systolic dysfunction with conventional echocardiography is not sufficiently sensitive to detect impaired myocardial function early in the course of the disease. Doppler myocardial imaging can quantify changes in global and regional longitudinal myocardial function with great precision. AIM: To identify parameters of cardiac dysfunction in patients with Fabry disease with no cardiac symptoms using conventional or Doppler echocardiography and tissue Doppler (including tissue tracking, strain and strain rate). METHODS: Four patients with Fabry disease (3 female; mean age 47 +/- 17 years) and 29 healthy controls (19 female and 10 male; mean age 38 +/- 14 years) were studied with conventional echocardiography and tissue Doppler imaging using a Vivid 7 scanner. The following parameters were measured: LV dimensions, ejection fraction (using Simpson's rule), systolic and diastolic velocities and tissue tracking of the mitral annulus at six sites (apical views). LV peak systolic strain and strain rate were obtained in 12 segments from apical views. RESULTS: Two patients had LV hypertrophy (one concentric and one apical). Diastolic impairment was detected in three patients by reduced flow propagation velocity of early transmitral flow (Vp) and E/Vp ratio. Mitral annulus systolic velocities were lower in Fabry disease than in the controls. Peak systolic strain and strain rate were diminished in all segments in three patients, showing impaired myocardial systolic function. The results are presented for each of the four patients. CONCLUSIONS: In patients with Fabry disease, with no cardiac symptoms and normal LV systolic function on conventional echocardiography, diastolic dysfunction was detected by Vp and E/Vp ratio regardless of LV hypertrophy. However, tissue Doppler imaging was able to detect impaired myocardial systolic function, particularly in patients with LV hypertrophy.

Adult↗
PubMed2004

Left ventricular diastolic dysfunction: risks, identification, and treatment.

Risk factors of cardiovascular disease, such as hypertension, diabetes, and myocardial infarction, if left untreated, will increase the risk of the development of chronic heart failure. Much is known about the pathophysiology and effective treatments of chronic heart failure from left ventricular systolic dysfunction; however, little clinical trial evidence exists concerning benefits of treating patients with chronic heart failure and preserved systolic function, also known as left ventricular diastolic dysfunction. Rather, an understanding of the pathophysiology and patient signs and symptoms has usually dictated choice of treatments. With the results of ongoing trials, as well as the Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM)-Preserved and the Digitalis Investigation Group (DIG) trials, clinical evidence is accumulating to support effective treatments in patients with left ventricular diastolic dysfunction. The focus of this review is to discuss the risks of, identification of, and rationale for therapeutic choices being employed for treating left ventricular diastolic dysfunction and implications from studies that may support these choices.

Adrenergic beta-Antagonists↗
PubMed1999

Estimation of pulmonary wedge pressure by transmitral Doppler in patients with chronic heart failure and atrial fibrillation.

Previous studies have demonstrated that left ventricular (LV) filling pressures can be estimated from transmitral Doppler recording in patients in sinus rhythm who have a broad spectrum of cardiac diseases. However, the correlation between pulmonary wedge pressure (PWP) and mitral Doppler profile has not yet been clearly defined in patients with atrial fibrillation, particularly in the presence of severe LV systolic dysfunction. The aim of this study was to evaluate the correlations between PWP and transmitral Doppler variables in patients with atrial fibrillation and chronic heart failure due to dilated cardiomyopathy. PWP and the mitral Doppler profile were simultaneously recorded in 35 consecutive heart failure patients (28 men, 7 women; mean age, 69 +/- 9 years) with severe LV dysfunction (mean ejection fraction 22% +/- 5%). Doppler measurements were averaged over 10 cardiac cycles. In addition, left atrial areas were derived from the apical 4-chamber view. Significant relations were observed between PWP and several parameters derived from the mitral flow: isovolumic relaxation time (r = -70), acceleration rate (r = 0.78), deceleration rate (r = 0.82), and deceleration time (r = -0.95). However, by stepwise multivariate analysis, deceleration time emerged as the sole independent predictor of PWP (r2 = 0.95, F = 590). The analysis led to the following equation: PWP = 51 - 0.26 (deceleration time). Our data suggest that mitral Doppler echocardiography is a useful tool for predicting PWP in heart failure patients with severe LV dysfunction even in the presence of atrial fibrillation.

Aged↗
PubMedDate not supplied

Effect of cardiac resynchronization therapy on diastolic dysfunction as assessed by transthoracic two-dimensional Doppler echocardiography.

Cardiac resynchronization therapy (CRT) in patients with left ventricular systolic dysfunction and electrical dyssynchrony has been shown to improve morbidity and mortality. Improvement in diastolic dysfunction may contribute to these results. In this retrospective study, the authors assessed the effect of CRT on the E/A ratio and mitral valve deceleration time, which are commonly utilized parameters of left ventricular diastolic function. In 13 patients (aged 62 +/- 11.3 years), the E/A ratio increased from 1.17 +/- 0.58 to 1.49 +/- 0.66 (p = nonsignificant) and the mitral valve deceleration time increased from 178.48+/-57.71 milliseconds to 227.70 +/- 76.18 milliseconds (p = 0.054) post-CRT. In patients without mitral regurgitation, there was a significant increase in E/A ratio, from 1.22 +/- 0.4 to 1.86 +/- 0.47 (p = 0.025), but no significant change in the mitral valve deceleration time post-CRT was observed. These data suggest improvement in diastolic dysfunction as assessed by routine two-dimensional echocardiography in patients who receive CRT devices.

Adult↗