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PubMed2003

Nonelectrocardiographic evidence that both ischemic preconditioning and adenosine preconditioning exist in humans.

OBJECTIVES: The objective of this study was to use electrocardiogram (ECG)-independent parameters to determine whether preconditioning (PC) exists in humans during percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Several studies suggest that both ischemia and adenosine induce PC in the human heart during PTCA. However, because almost all of these studies relied on ST-segment shifts as indicators of the severity of ischemia, their conclusions continue to be questioned, and the very existence of ischemic or adenosine PC in humans remains controversial. METHODS: Eighteen patients received either intracoronary adenosine (n = 9) or normal saline (n = 9); 10 min later, they underwent PTCA (three 2-min balloon inflations 5 min apart). RESULTS: Compared with the first inflation, in untreated patients the second and third inflations were associated with less systolic dysfunction (two-dimensional echocardiography), less diastolic dysfunction (color M-mode echocardiography), less lactate production, and less H(+) release into the great cardiac venous blood. In adenosine-treated patients, the extent of all of these abnormalities during the first inflation was less than in untreated patients and did not change with subsequent inflations. CONCLUSIONS: Previous exposure to a brief episode of ischemia (first balloon inflation) or to adenosine produces concordant decreases in ECG, subjective, mechanical, and metabolic manifestations of ischemia during PTCA. These data support the concept that both ischemic PC and pharmacologic PC exist in humans and that PTCA is a useful clinical setting in which to discern their mechanism.

Adenosine↗
PubMed1997

Relationship between left ventricular diastolic function and atrial natriuretic factor in never-treated mild hypertensives.

Using digitized M-mode echocardiograms, we evaluated the relationship between plasma atrial natriuretic factor (ANF) and morphofunctional characteristics of the left ventricle (LV) in 24 mild hypertensive men, never treated, with normal renal function. For each subject we collected a blood sample for plasma ANF evaluation and, immediately after, we recorded the LV echocardiogram. All the patients had normal LV diastolic diameter and systolic function; LV hypertrophy was present in 10 patients, 7 of whom had left atrial enlargement, and 13 patients had impaired LV diastolic function. ANF was similar between patients with and without LV hypertrophy, as well as between patients with and without left atrial enlargement, whereas ANF was significantly (P < .01) higher in patients with LV diastolic dysfunction than in patients with normal diastolic function. ANF was inversely correlated with both indices of diastolic function (peak lengthening rate and peak wall thinning rate), whereas it did not correlate with blood pressure, heart rate, end-systolic wall stress, and other LV parameters. In conclusion, from our results, ANF level in never-treated mild hypertensives is related neither to the degree of LV hypertrophy nor to the afterload, expressed as blood pressure or end-systolic wall stress, whereas it is mainly influenced by LV diastolic function: the diastolic impairment induces an increase in ANF level, probably through an increased atrial stretch.

Adult↗
PubMed2003

Beta-blocker treatment of patients with diastolic heart failure and arterial hypertension. A prospective, randomized, comparison of the long-term effects of atenolol vs. nebivolol.

We compared the effects of 6 months administration of atenolol or nebivolol on resting and exercise hemodynamic parameters and maximal exercise capacity, in 26 patients with hypertension and left ventricular (LV) diastolic dysfunction (ejection fraction >50%, end-diastolic diameter <60 mm and increased pulmonary wedge pressure at rest and/or at peak exercise). Both atenolol and nebivolol administration was associated with a significant decrease in the resting and peak exercise heart rate and blood pressure and in LV mass, with an increase in the E/A ratio. This latter effect was greater with nebivolol. Nebivolol was associated with an increase in the peak VO(2), VO(2) at the anaerobic threshold and with a decrease in the VE/VCO(2) ratio. With regards to the hemodynamic parameters, compared to patients on atenolol, those on nebivolol showed a lower reduction in the cardiac index, a greater increase in the stroke volume index and a decline in the mean pulmonary artery pressure and pulmonary wedge pressure, both at rest and peak exercise. Thus, although the two beta-blockers have a similar antihypertensive action, nebivolol administration was associated with a greater hemodynamic improvement, compared to atenolol.

Adrenergic beta-Antagonists↗
PubMed2003

Diastolic heart failure in older people.

OBJECTIVES: To determine the prevalence of diastolic heart failure in older people in the community, identify associated risk factors and measure its impact on function and quality of life. DESIGN: Cross-sectional population-based study. METHODS: A two-stage random sample of 500 subjects was drawn from 5,002 subjects aged 70 years and over living at home. Diastolic heart failure was diagnosed by a panel of three physicians, based on clinical assessment and echocardiographic indicators of diastolic dysfunction. MAIN OUTCOME MEASURES: Prevalence of diastolic heart failure and its effect on function and quality of life as measured by Nottingham Extended Activities of Daily Living, Hospital Anxiety and Depression and SF-36 questionnaires. RESULTS: The prevalence of diastolic heart failure was 5.54% (95% CI = 3.71, 7.87) and was higher in women (8.32%) than in men (1.25%), P = 0.008. On multivariate analysis of variance, diastolic heart failure was associated with female gender and history of ischaemic heart disease. Subjects with diastolic heart failure had significantly poorer functional status and physical health than those without heart failure. CONCLUSIONS: Diastolic heart failure is relatively common in older people and is associated with adverse affects in older people's lives.

Activities of Daily Living↗
PubMed1989

Diastolic function after cardiac and heart-lung transplantation.

The mechanical efficiency of left ventricular contraction and relaxation, the asynchrony of the onset of left ventricular relaxation, the time constant of left ventricular isovolumic pressure decay, and left ventricular chamber and myocardial stiffness were analysed in 32 patients after cardiac (24) and heart-lung transplantation (8). After cardiac transplantation left ventricular myocardial stiffness was increased and a mild degree of incoordinate contraction and relaxation was seen. In contrast, after heart-lung transplantation diastolic function was almost normal. Impairment of passive diastolic properties was significantly related to the ischaemic time of the donor heart and the donor's age. The index of left ventricular asynchrony was related to the ischaemic time and the recipient's age. The interval between transplantation and study did not influence the number of rejection episodes. This study confirms the presence of diastolic dysfunction after cardiac transplantation. Impairment of diastolic function seems to be related to the ischaemic time of the donor heart and to a mismatch between the size of the donor heart and the recipient's needs.

Adolescent↗
PubMed2001

Aldosterone production is activated in failing ventricle in humans.

BACKGROUND: Recent reports have indicated that aldosterone is produced in extra-adrenal tissues in animals. The present study was designed to examine whether aldosterone is produced in human heart. METHODS AND RESULTS: Plasma levels of aldosterone, BNP, and angiotensin-converting enzyme were measured in anterior interventricular vein (AIV), coronary sinus (CS), and aortic root (Ao), respectively, in 20 patients with left ventricular systolic dysfunction (LVSD), 25 patients with LV diastolic dysfunction (LVDD), and 23 control subjects. Aldosterone levels were significantly higher in AIV and CS than Ao in LVSD (98+/-10 versus 72+/-9 pg/mL, P:<0.001, and 97+/-11 versus 72+/-9 pg/mL, P:<0.001, respectively) and LVDD (87+/-10 versus 71+/-9 pg/mL, P:<0.01, and 84+/-10 versus 71+/-9 pg/mL, P:<0.01, respectively) groups, but no differences were observed in levels for these sites in the control group. Levels of ACE activity and BNP also were higher in AIV than Ao in both LV dysfunction groups. The difference in aldosterone levels between AIV and Ao and those in BNP and angiotensin-converting enzyme had a significant positive correlation with LVEDP and a significant negative correlation with LV ejection fraction in the LVSD group. CONCLUSIONS: Production of aldosterone, angiotensin-converting enzyme, and BNP are activated in failing human ventricle in proportion to severity.

Adult↗
PubMed2006

Impaired cardiac contractile function in ventricular myocytes from leptin-deficient ob/ob obese mice.

The level of the obese gene product leptin is often positively correlated with body weight, supporting the notion that hyperleptinemia contributes to obesity-associated cardiac dysfunction. However, a link between leptin levels and cardiac function has not been elucidated. This study was designed to examine the role of leptin deficiency (resulting from a point mutation of the leptin gene) in cardiomyocyte contractile function. Mechanical properties and intracellular Ca(2+) transients were evaluated in ventricular myocytes from lean control and leptin-deficient ob/ob obese mice at 12 weeks of age. Cardiac ultrastructure was evaluated using transmission electron microscopy. ob/ob mice were overtly obese, hyperinsulinemic, hypertriglycemic, hypoleptinemic and euglycemic. Ultrastructural examination revealed swelling and disorganization of cristae in mitochondria from ob/ob mouse ventricular tissues. Cardiomyocytes from ob/ob mice displayed reduced expression of the leptin receptor Ob-R, larger cross-sectional area, decreased peak shortening and maximal velocity of shortening/relengthening, and prolonged relengthening but not shortening duration compared with lean counterparts. Consistent with mechanical characteristics, myocytes from ob/ob mice displayed reduced intracellular Ca(2+) release upon electrical stimulus associated with a slowed intracellular Ca(2+) decay rate. Interestingly, the contractile aberrations seen in ob/ob myocytes were significantly improved by in vitro leptin incubation. Contractile dysfunction was not seen in age- and gender-matched high fat-induced obese mice. These results suggested that leptin deficiency contributes to cardiac contractile dysfunction characterized by both systolic and diastolic dysfunction, impaired intracellular Ca(2+) hemostasis and ultrastructural derangement in ventricular myocytes.

Animals↗
PubMed2005

Left heart lesions in patients with Ebstein anomaly.

OBJECTIVE: To identify the incidence of left heart abnormalities in patients with Ebstein anomaly, recognizing that left-sided lesions in this patient group have been overlooked. PATIENTS AND METHODS: According to the echocardiography database at the Mayo Clinic in Rochester, Minn, 106 consecutive patients with Ebstein anomaly underwent echocardiography between July 1, 2001, and February 28, 2003. Clinical data as well as electrocardiographic and echocardiographic reports and images were reviewed. RESULTS: Ebstein anomaly was severe in 76 patients (72%). Previous tricuspid valve surgery was reported in 46 patients (43%), and previous closure of an atrial septal defect or patent foramen ovale was reported in 34 patients (32%). Left ventricular (LV) myocardial changes resembling noncompaction occurred in 19 patients (17.9%), LV systolic dysfunction in 7 patients (7%), LV diastolic dysfunction in 34 (36%) of 95 patients, and LV dilatation in 4 patients (4%). Additional left-sided cardiac lesions included mitral valve prolapse in 16 patients (15%), bicuspid aortic valve in 8 (8%), mitral valve dysplasia in 4 (4%), and ventricular septal defect in 8 (8%). Wolff-Parkinson-White syndrome occurred in 22 patients (21%). The QRS axis tended to be different in LV noncompaction with a mean +/- SD axis of 12 degrees +/- 74 degrees vs 36 degrees +/- 66 degrees overall (P=.08). Otherwise, there were no differences in clinical or surgical data between the groups with normal and abnormal LV myocardium. CONCLUSIONS: In patients with Ebstein anomaly, left heart abnormalities involving the myocardium or valves were observed in 39% of patients. Ebstein anomaly should not be regarded as a disease confined to the right side of the heart.

Adolescent↗
PubMed2004

[Structural and functional cardiac changes and sex hormone levels in men with sexual dysfunctions].

44 men with chronic prostatitis were examined for structural-functional heart alterations with reference to severity of erectile dysfunction (ED). Sex hormones were also estimated. Control group consisted of 20 healthy men. Doppler echocardiography, 24-h monitoring of arterial pressure (AP) and ECG, finger and ultrasound investigation of the prostatic gland and microscopy of its secretion were made. Blood plasm testosteron, prolactin and dehydroepiandrosterone-sulphate were estimated by enzyme immunoassay. Erectile function was assessed by the questionnaire "International index of erectile function". Thus, sexual hormone changes associated with sexual dysfunction in men promote left ventricular diastolic dysfunction. The type of intracardiac hemodynamics in this case is, as a rule, restrictive.

Adult↗
PubMed1998

Recognized molecular mechanisms of heart failure: approaches to treatment.

Abnormalities of cytosolic calcium handling and myocyte energetics appear to play an important role in mediating contractile dysfunction in heart failure. Systolic and diastolic dysfunction in the failing heart are related to abnormalities of the excitation-contraction mechanism as well as myofilament calcium sensitivity. These abnormalities can be viewed as a compensatory mechanism as the myocytes by down regulating its function and metabolic activity preserve energy consumption and allow better maintenance of basal cellular homeostasis. The end point of myocyte dysfunction, however, is a reduced contraction, which, in turn, might cause a reduced cardiac output and a threatening of arterial pressure. This causes a second level of adaptation, which implies a neuroendocrine response of the whole organism. Consequently, the syndrome of congestive heart failure is characterized not only by impaired ventricular function, but also by an increase in some endogenous substances leading to vasoconstriction and water and salt retention. Although activation of the systems that release these substances is presumed to be compensatory, the sympathetic nervous system and renin-angiotensin-aldosterone system as well as the endothelins may contribute to the pathogenesis of the syndrome. Opposite to the effects of these systems are those evoked by the release of atrial natriuretic peptides. The peptides exert a potent direct vasodilatation and natriuresis. In addition, atrial natriuretic peptides inhibit the release of norepinephrine from nerve terminals and suppress the formation of renin. However, the natriuretic and vasodilator effects of these peptides in patients with congestive heart failure are outweighed by the sodium retention and vasoconstriction caused by sympathetic stimulation and activation of the renin-angiotensin-aldosterone system. The reasons for this are not entirely known. The atrial stretch receptors that are responsible for the release of the atrial peptides become impaired, and it has been suggested that patient with heart failure may adapt to the physiologic effects of atrial natriuretic peptides. The possibility that congestive heart failure is in part a humoral disease is reviewed here and consequently pharmacologic treatment aimed at reducing the effects of the neuroendocrine response as to be advantageous for patients with heart failure.

Animals↗
PubMed1999

No evidence for systolic or diastolic left ventricular dysfunction at rest in selected patients with long-term type I diabetes mellitus.

We assessed left ventricular systolic and diastolic function using pulsed-waved Doppler echocardiography in a selected group of 20 patients with insulin-dependent diabetes mellitus (IDDM) (mean age, 35 +/- 8 years; mean diabetes duration, 17 + 7 years). Our patients were free of autonomic neuropathy and major micro- or macrovascular complications and had no evidence of ischemic heart disease or hypertension. The results were compared with those of 20 age- and sex-matched control subjects. We found that left ventricular geometry and mass, systolic function by M-mode and 2D-echocardiography, isovolumetric relaxation time, deceleration time and the PEP/LVET ratio were not significantly different between patients and control subjects. Hemodynamic parameters were also not significantly different except for a slightly higher heart rate in the patient group (75 +/- 11 vs. 68 + 6 bpm, P = 0.019). After correction of A-peak velocities for differences in heart rate, there was no significant difference of Doppler indices of diastolic left ventricular function between patients and control subjects. The absence of significant left ventricular systolic and diastolic dysfunction by Doppler echocardiography in our study patients may be explained by our patient selection. Left ventricular dysfunction in diabetic patients without concomitant hypertensive or ischemic heart disease may only occur in conjunction with microvascular disease in other organ systems, with autonomic neuropathy or with poor metabolic control.

Adult↗
PubMed2006

Persistent and reversible cardiac dysfunction among amateur marathon runners.

AIMS: Transient systolic and diastolic abnormalities in ventricular function have previously been documented during endurance sports. However, these described alterations may be limited by the techniques applied. We sought, using less load-dependent methods, to characterize both the extent and the chronology of the cardiac changes associated with endurance events. METHODS AND RESULTS: Transthoracic echocardiography (TTE) was performed prior to, immediately after, and approximately 1 month after completion of the 2003 Boston Marathon in 20 amateur athletes. TTE included two-dimensional, spectral and tissue Doppler (TD) and flow propagation velocity (V(p)). After completion of the marathon, global measures of left ventricular (LV) systolic function were unchanged (EF 59 +/- 6 vs. 61 +/- 4% post, P = 0.14), whereas TD-derived measures of LV systolic function [septal strain -23 +/- 5 vs. -17 +/- 4%, P = 0.007; septal strain rate (SR) -1.5 +/- 0.3 vs. -1.1+/- 0.2 s(-1), P = 0.007] and right ventricular (RV) systolic function (RV apical strain -33 +/- 4 vs. -27 +/- 5%, P = 0.001; RV apical SR -2.4 +/- 0.7 vs. -1.8 +/- 0.5, P = 0.002) were reduced. Significant changes in transmitral velocity (E/A ratio 2.0 +/- 0.5 vs.1.3 +/- 0.3, P = 0.005) and TD indices of LV and RV diastolic function (E(a) septal 9.5 +/- 1.8 vs. 8.1 +/- 1.2 cm/s post-marathon, P = 0.01) were also observed, indicating an inherent alteration in LV relaxation. Although all indices of LV and RV systolic function had returned to normal on follow-up, there were persistent diastolic abnormalities (RV E(a), 11.5 +/- 1.5 cm/s pre-marathon vs. 10.0 +/- 1.6 cm/s follow-up, P = 0.01). CONCLUSION: Marathon running leads to transient systolic and more persistent diastolic dysfunction of both the LV and the RV.

Adult↗
PubMed1998

Effects of hypoproteinemia-induced myocardial edema on left ventricular function.

In previous studies, we observed left ventricular (LV) systolic and diastolic dysfunction in association with interstitial myocardial edema (IME) induced by either coronary venous hypertension (CVH) or lymphatic obstruction. In the present study, we examined the effects of myocardial edema induced by acute hypoproteinemia (HP) on LV systolic and diastolic function. We also combined the methods of HP and CVH (HP-CVH) to determine their combined effects on LV function and myocardial water content (MWC). We used a cell-saving device to lower plasma protein concentration in HP and HP-CVH groups. CVH was induced by inflating the balloon in the coronary sinus. Six control dogs were treated to sham HP. Conductance and micromanometer catheters were used to assess LV function. Contractility, as measured by preload recruitable stroke work, did not change in control or HP groups but declined significantly (14.5%) in the HP-CVH group. The time constant of isovolumic LV pressure decline (tau) increased significantly from baseline by 3 h in the HP (24.8%) and HP-CVH (27.1%) groups. The end-diastolic pressure-volume relationship (stiffness) also increased significantly from baseline by 3 h in the HP (78.6%) and HP-CVH (42.6%) groups. Total plasma protein concentration decreased from 5.2 +/- 0.2 g/dl at baseline to 2.5 +/- 0.0 g/dl by 3 h in the HP and HP-CVH groups. MWC of the HP (79.8 +/- 0.25%) and HP-CVH groups (79.8 +/- 0.2%) were significantly greater than that of the control group (77.8 +/- 0.3%) but not different from one another. In conclusion, hypoproteinemia-induced myocardial edema was associated with diastolic LV dysfunction but not systolic dysfunction. The edema caused by hypoproteinemia was more than twice that produced by our previous models, yet it was not associated with systolic dysfunction. CVH had a negative inotropic effect and no significant influence on MWC. IME may not have the inverse causal relationship with LV contractility that has been previously postulated but appears to have a direct causal association with diastolic stiffness as has been previously demonstrated.

Acid-Base Equilibrium↗
PubMed2006

Acromegaly and the cardiovascular system.

Acromegaly is characterized by an increased cardiovascular morbidity and mortality. In fact, growth hormone and insulin-like growth factor-I excess induces a specific cardiomyopathy. The heart is involved from the very early stages of the disease in which the hyperkinetic syndrome (high heart rate and increased systolic output) takes place. Frequently, if the disease is untreated for many years or unsuccessfully treated, concentric biventricular hypertrophy and diastolic dysfunction can develop and, at least, lead to diastolic congestive heart failure. Rhythm disturbances and valve dysfunction are also frequently described in acromegaly. The coexistence of other complications, such as diabetes and arterial hypertension, can induce the worsening of acromegalic cardiomyopathy. Control of acromegaly by surgery or pharmacotherapy could improve cardiovascular morbidity thanks to decreasing left ventricular mass and reducing cardiac dysfunction. In conclusion, an early diagnosis and a careful evaluation of cardiac function, morphology and activity seem to be mandatory in acromegaly.

Acromegaly↗
PubMed2004

Plasma B-type natriuretic peptide levels in systolic heart failure: importance of left ventricular diastolic function and right ventricular systolic function.

OBJECTIVES: This study was designed to characterize the importance of echocardiographic indexes, including newer indexes of diastolic function, as determinants of plasma B-type natriuretic peptide (BNP) levels in patients with systolic heart failure (SHF). BACKGROUND: Plasma BNP levels have utility for diagnosing and managing heart failure. However, there is significant heterogeneity in BNP levels that is not explained by left ventricular size and function alone. METHODS: In 106 patients with symptomatic SHF (left ventricular ejection fraction [LVEF] <0.35), we measured plasma BNP levels and performed comprehensive echocardiography with assessment of left ventricular diastolic function, including color M-mode (CMM) and tissue Doppler imaging (TDI), and of right ventricular (RV) function. RESULTS: Median plasma BNP levels were elevated and increased with greater severity of diastolic dysfunction. We found significant correlations (p < 0.001 for all) between BNP and indexes of myocardial relaxation (early diastolic velocity: r = -0.26), compliance (deceleration time: r = -0.55), and filling pressure (early transmitral to early annular diastolic velocity ratio: r = 0.51; early transmitral flow to the velocity of early left ventricular flow propagation ratio: r = 0.41). In multivariate analysis, overall diastolic stage, LVEF, RV systolic dysfunction, mitral regurgitation (MR) severity, age and creatinine clearance were independent predictors of BNP levels (model fit r = 0.8, p < 0.001). CONCLUSIONS: Plasma BNP levels are significantly related to newer diastolic indexes measured from TDI and CMM in SHF. Heterogeneity of BNP levels in patients with SHF reflects the severity of diastolic abnormality, RV dysfunction, and MR in addition to LVEF, age, and renal function. These findings may explain the powerful relationship of BNP to symptoms and prognosis in SHF.

Aged↗
PubMed2006

N-terminal pro B-type natriuretic peptide levels: correlation with echocardiographically determined left ventricular diastolic function in an ambulatory cohort.

OBJECTIVES: To investigate the correlations of plasma N-terminal pro B-type natriuretic peptide (NT-proBNP) levels with echocardiographic measurements of left ventricular (LV) systolic and/or diastolic function. BACKGROUND: Plasma levels of NT-proBNP are increased in heart failure. The extent to which NT-proBNP levels increase in LV diastolic dysfunction has not been well characterized. METHODS: Plasma NT-proBNP levels were measured in 191 consecutive, clinically stable, ambulatory patients. Echocardiography was used to determine LV systolic (LV ejection fraction [LVEF]) and diastolic function by mitral E wave to Doppler tissue early diastolic lateral annulus velocity ratio (E/Em). Patients with a history, physical findings, and/or echocardiographic evidence of cardiovascular disease (n = 148) were grouped as: (1) normal LV systolic function (LVEF > or = 55%, n = 81); and (2) LV systolic dysfunction (LVEF < 55%, n = 67). They were compared to a group of healthy control subjects (n = 43). Multivariate regression analyses were used to determine significant correlations with plasma NT-proBNP levels. RESULTS: NT-proBNP levels correlated negatively with LVEF (P < .001) and positively with E/Em (P = .001). Multivariate regression analysis demonstrated a significant correlation of NT-proBNP levels with LVEF (P < .001) and E/Em (P = .03). CONCLUSIONS: In this clinically stable, ambulatory cohort of patients with cardiovascular disease and healthy control subjects, plasma NT-proBNP levels were significantly higher in those with LV systolic dysfunction and/or elevated filling pressures, independent of the effects of LV mass, renal function, and age. These results suggest that NT-proBNP levels may be a useful adjunct in the characterization of patients presenting with history and/or symptoms compatible with LV systolic and/or diastolic dysfunction.

Ambulatory Care↗
PubMed2001

Reversible impairment of left and right ventricular systolic and diastolic function during short-lasting atrial fibrillation in patients with an implantable atrial defibrillator: a tissue Doppler imaging study.

AF with a fast ventricular response may cause ventricular mechanical impairment, though whether short-lasting AF with satisfactory rate control may affect ventricular function is unknown. This study investigated if prompt cardioversion by an implantable atrial defibrillator (IAD) may prevent left (LV) and right ventricular (RV) systolic and diastolic dysfunction. Ten patients (mean age 61 +/- 9 years, 8 men) with paroxysmal AF without structural heart disease who received an IAD were studied by echocardiography and tissue Doppler imaging (TDI) for both ventricles. Measurements were made during baseline sinus rhythm and at 1-minute, 20-minute, 4-hour, and 1-week postcardioversion of an episode of spontaneous AF. The occurrence of AF and the ventricular rate were monitored at 2-hour intervals by the device. There were 50 episodes of AF with a mean duration of 8.8 +/- 8.9 days (2 hours to 37 days). There was no difference in M-mode measured LV fractional shortening and ejection fraction between baseline sinus rhythm and after cardioversion. However, the TDI derived myocardial systolic velocity (TDI-S) was significantly lower at 1-minute postcardioversion and was normalized at 1 week in both LVs (baseline: 5.7 +/- 1.8, 1 minute: 4.2 +/- 1.0, 20 minutes: 4.3 +/- 0.9, 4 hours: 4.8 +/- 1.0, 1 week: 5.5 +/- 1.8 cm/s; P < 0.005 when comparing 1 minute and 20 minutes to baseline; P < 0.05 when comparing 4 hour to baseline) and RV (baseline: 10.4 +/- 2.1, 1 minute: 7.8 +/- 1.4, 20 minutes: 8.1 +/- 1.2, 4 hours: 9.2 +/- 1.5, 1 week: 10.0 +/- 2.0 cm/s; P < 0.005 when comparing 1 minute, 20 minutes, and 4 hours to baseline). For diastolic function, transmitral Doppler study showed a decrease in early filling velocity at 1 minute (P < 0.05) and 20 minutes (P < 0.005), which was normalized at 4 hours. There was no change in transtricuspid Doppler flow. However, TDI derived myocardial early filling velocity was decreased in the LV (baseline: 6.0 +/- 2.8, 1 minute: 5.4 +/- 2.3, 20 minutes: 5.4 +/- 2.1, 4 hours: 6.1 +/- 2.2, 1 week: 5.8 +/- 1.7 cm/s; P < 0.05 when comparing 1 minute and 20 minutes to baseline) and RV (baseline: 8.9 +/- 3.5, 1 minute: 7.9 +/- 3.3, 20 minutes: 8.1 +/- 3.3, 4 hours: 8.5 +/- 2.9, 1 week: 8.4 +/- 3.5 cm/s; P < 0.05 when comparing 1 minute to baseline). AF of a longer duration (> 48 hours) resulted in a more depressed TDI-S in LV (> 48 hours: 4.2 +/- 1.0, < or = 48 hours: 5.3 +/- 1.3 cm/s; P < 0.01). Shocks in sinus rhythm did not affect any of the above echocardiographic parameters. Therefore, despite adequate rate control, short-lasting AF impairs systolic and diastolic function in both ventricles, which improves gradually after cardioversion. Early restoration of sinus rhythm by an IAD minimizes ventricular dysfunction. TDI is a sensitive tool to assess early systolic and diastolic dysfunction.

Atrial Fibrillation↗
PubMed2003

Comparison of pulmonary venous flow velocities and left ventricular diastolic and ejection time in patients with moderate mitral and aortic stenosis. Pulmonary venous flow velocities in mitral and aortic stenosis.

BACKGROUND: Doppler pulmonary venous flow velocities (PVFV) pattern are useful parameters in assessing the left ventricular diastolic functions. Both mitral stenosis (MS) and aortic stenosis (AS) lead to diastolic dysfunction. We compared PVFV and left ventricular diastolic and ejection time (ET) in patients with moderate MS and AS. METHODS: Forty-three patients with moderate MS (group 1), 65 patients with moderate AS (group 2), and 33 healthy subjects as controls (group 3) were included in this study. After obtaining standard measurements echocardiographically, diastolic period (DP), ET, the ratio of the DP to the ET (DP/ET), isovolumetric contraction time (ICT), isovolumetric relaxation time (IRT), peak systolic flow velocity (PS), peak antegrade diastolic flow velocity (PD), peak reversal flow velocity at atrial contraction (PRA), the ratio of the peak systolic to the diastolic flow velocity (PS/PD), deceleration time of the antegrade diastolic flow (PDDT), and pressure half time of the peak antegrade diastolic flow velocity (PDPHT) were measured. Mitral valve area (MVA), aortic valve area (AVA), systolic pulmonary artery pressure (PAP), peak and mean gradients were calculated with standard formulas. RESULTS: In univariate analysis, MVA was correlated with PDPHT and PDDT (r = -0.41; p < 0.01, r = -0.36; p < 0.05, respectively), also it was correlated with DP/ET (r = -0.57; p < 0.001). Mitral peak and mean diastolic gradient were correlated with PS/PD (r = -0.43; p < 0.01, r = -0.36; p < 0.05, respectively) and DP/ET (r = 0.51; p < 0.01, r = 0.46; p < 0.01, respectively). AVA was only correlated with DP/ET (r = 0.38; p < 0.05). Aortic peak and mean systolic gradient were correlated with PS/PD (r = -0.29; p < 0.05, r = -0.27; p < 0.05, respectively) and DP/ET (r = -0.38; p < 0.01, r = -0.40; p < 0.01, respectively). In the same analysis, PAP in patients in group 1 and 2 was correlated with PS/PD (r = -0.42; p < 0.01 and r = -0.40; p < 0.01, respectively) and also it was correlated with PD (r = 0.37; p < 0.05 and r = 0.27; p < 0.05, respectively) in both groups. CONCLUSION: Moderate MS and AS similarly affect the PVFV, and PS/PD correlates with hemodynamics similarly both in MS and AS. Nevertheless, PDDT and PDPHT correlate with solely MVA. IRT higher in AS than MS, though DP/ET and ICT higher in MS than AS, and DP/ET relates with the severity of both MS and AS.

Adult↗