Diastolic Transmitral Flow Research Articles

Effect of acute alterations in afterload on left ventricular function in patients with combined coronary artery and peripheral vascular disease.

To assess the effect of acute alterations in afterload by aortoiliac clamping, during peripheral vascular surgery, on left ventricular function. Prospective examination of the left ventricular long axis and transmitral Doppler flow preoperatively and intraoperatively; before aortic clamping, during clamping and 5 min, 15 min, and 5 days after unclamping. A tertiary referral centre for cardiac and vascular disease equipped with invasive and non-invasive facilities. 20 patients (11 men; mean (SD) age 61 (8) years) with significant aortoiliac disease and documented coronary artery disease and 21 normal controls of similar age. Preoperatively: long axis function was abnormal compared with that in normal controls. In systole total long axis excursion and peak shortening rate were reduced, onset of shortening delayed, and there was pre-ejection lengthening (P < 0.001). In diastole there was abnormal shortening during isovolumic relaxation, delaying the onset of long axis lengthening (P < 0.001). Peak lengthening rate was also reduced and A wave excursion increased (P < 0.001). Transmitral Doppler showed increased A wave velocity and reduced peak E/A diastolic flow velocities ratio (P < 0.001). Intraoperatively: preclamping results did not differ from those before operation. With clamping the extent of systolic and diastolic abnormalities promptly increased as to a lesser extent did those of transmitral flow velocity, although heart rate and blood pressure did not change significantly. Total long axis excursion and A wave amplitude were more reduced by aortic than iliac clamping, whereas the onset of lengthening was more delayed and the lengthening velocity more reduced with iliac clamping. Some 5 min after unclamping systolic long axis function had already returned towards normal; total excursion increased, as did the peak shortening rate, and the onset of shortening became less delayed (P < 0.001). In diastole the delayed onset of lengthening regressed, its lengthening velocity increased, and A wave excursion fell (P < 0.001). Early diastolic transmitral flow velocity also increased. This improvement in systolic and diastolic long axis function had progressed 15 min after unclamping but showed no further change at 5 days. At 5 days after operation, however, systolic and diastolic measurements had improved compared with those preoperatively. Resting left ventricular long axis function is abnormal in patients with combined coronary artery disease and peripheral vascular disease. It is unaffected by anaesthesia but deteriorates with aortic or iliac clamping, although blood pressure remains unchanged. It promptly improves with unclamping after successful peripheral arterial reconstruction. Thus, even in apparently stable coronary artery disease, resting subendocardial function is labile, showing pronounced alterations with changing after-load, even when arterial pressure itself does not change.

Difference Between Deceleration Time of Early Transmitral and Pulmonary Venous Diastolic Flow in Patients with Hypertension

Difference Between Deceleration Time of Early Transmitral and Pulmonary Venous Diastolic Flow in Patients with Hypertension

Circadian variation of left ventricular diastolic function in healthy people.

To assess whether left ventricular function shows circadian variation in healthy people. 10 healthy men (7) and women (3) aged 35-50 underwent M mode echocardiography of the left ventricle and Doppler velocimetry of transmitral flow at 4 h intervals over 24 h. The participants were in hospital over the study period and their diet, meal times, and sleeping hours were standardised as far as possible. Heart rate, blood pressure, left ventricular and atrial diameters, fractional shortening, peak early and late transmitral velocities, time from the second heart sound to the early diastolic velocity peak (relaxation time), isovolumic relaxation period, acceleration and deceleration of the early transmitral flow, atrial filling fraction. A circadian rhythm was observed in heart rate and blood pressure, but neither the left ventricular diameters and systolic function nor the left atrial size showed statistically significant diurnal trends. The relaxation time (mean (SD)) measured 144 (16) ms at 2 pm, 144 (21) ms at 6 pm, 149 (22) ms at 10 pm, 168 (23) ms at 2 am, 174 (28) ms at 6 am, and 151 (21) ms at 10 am (P = 0.009). Diurnal rhythms were seen also in the isovolumic relaxation period (P = 0.003) and in the acceleration of the early diastolic transmitral flow (P = 0.037); the lowest and highest values of flow acceleration were observed during the nocturnal and daytime hours, respectively. The Doppler indices of left ventricular filling in healthy people show diurnal changes suggestive of a circadian rhythm in the rate of left ventricular relaxation. The most likely underlying mechanism is the day-night cycle in sympathoadrenal activity.

A new scoring system, using Doppler transmitral diastolic measurement, identifies transient myocardial ischaemia.

In patients with acute transient myocardial ischaemia, changes in left ventricular filling produce alterations in transmitral diastolic flow velocity and isovolumic relaxation time. In this study a scoring system derived from isovolumic relaxation time and indices from transmitral flow velocity was used to evaluate perioperative transient myocardial ischaemia. Fifty three patients with known coronary artery disease or at risk were studied. Ischaemic events were assessed using Doppler transoesophageal echocardiography midoesophageal left ventricular four-chamber view planes. Diastolic Doppler ratios of peak early to atrial peak (E/A), deceleration time, deceleration rate and isovolumic relaxation time were scored using standard methods. An evaluation of peri-operative ischaemic events could be important for patients with a non-ischaemic cause for abnormal segmental wall motion, as the use of a two-dimensional scoring system has limitations. Acute changes in the Doppler ratio of peak early to atrial peak must be interpreted cautiously during surgery. Diastolic dysfunction commonly occurs during ischaemia and recognition of this may alter the approach to monitoring as well as to treatment.

Left ventricular diastolic function after anthracycline chemotherapy in childhood: relation with systolic function, symptoms, and pathophysiology.

To examine left ventricular (LV) diastolic function in patients previously treated with anthracycline drugs for childhood malignancy. To consider clinical relevance, relations with systolic dysfunction, and the pathophysiology of anthracycline cardiotoxicity. Cross sectional echocardiographic study of LV function. Supraregional centre for paediatric cardiology, principal centre for the treatment of childhood malignancy in southwest England. 226 of 236 patients surviving between 6.5 months and 17 (median 5.3) years from initial anthracycline treatment for childhood malignancy attended for clinical and echocardiographic examination. Cumulative anthracycline doses were between 50 and 750 (median 300) mg/m2. 22 patients had also received cardiac irradiation. Detailed assessment of transmitral diastolic pulsed wave Doppler flow patterns along with LV dimensions and systolic function measured by M mode echocardiography. Peak early (E) and atrial (A) phase filling velocities and EA ratio, time and acceleration and deceleration to and from peak E velocity, velocity integrals and ratio, isovolumic relaxation time (IVRT), and heart rate were measured. Results were examined in relation to LV cavity and posterior wall dimensions and shortening fraction (SF), and compared with paired control data matched for body surface area. Eleven (5%) patients had abnormal effort tolerance. Fifty one (23%) had SF < 30% and SF was inversely correlated with cumulative dose and time from treatment. The relative risk of symptomatic cardiac failure was greatly increased by prior irradiation; > 60% of irradiated patients who received > 400 mg/m2 of anthracycline were symptomatic. Early diastolic filling was relatively normal or enhanced at low anthracycline doses or when SF was preserved, with a shorter IVRT and increased atrial phase filling. Early filling was reduced at higher doses or with reduced SF, with longer IVRT and a further increase in atrial phase filling. A more "restrictive" pattern of diastolic filling (with high E and low A velocities) was seen in some patients, particularly after cardiac irradiation. Significant abnormalities of diastolic function are associated with anthracycline induced cardiac damage. These are not linearly related to anthracycline dose but appear to reflect the underlying myocardial pathophysiology associated with anthracycline toxicity, which is not demonstrated by the standard M mode echocardiogram. Although the overall clinical significance of such diastolic dysfunction is uncertain, some individual abnormalities may have significant management and therapeutic implications.

Severe diastolic dysfunction after endoventriculoplasty

Endoventriculoplasty with pericardial patch has been advocated to repair anteroseptal ventricular aneurysm, but no studies have reported the influence of this technique on diastolic left ventricular function. We have evaluated the changes on ventricular filling by means of pulsed Doppler recording of diastolic transmitral flow. Doppler analysis reveals three distinct spectral patterns: (1) normal, (2) inverted, and (3) restrictive. We have found an abrupt change from a preoperative normal to postoperative restrictive pattern in a significant minority of patients (8%) who underwent endoventriculoplasty. These patients had clinical and hemodynamic signs (New York Heart Association class, time from anterior myocardial infarction, left ventricular end-diastolic pressure, pulmonary hypertension, and mitral regurgitation) of severe impairment but no differences were found in ejection fraction, aneurysmal extension, or remote myocardial function. Moreover, after operation they had a satisfactory ejection fraction, a low end-diastolic volume, and an apex-base length shorter than the predicted value for a normal population. The presence of a postoperative restrictive pattern of diastolic filling is a strong predictor of 3-month mortality and makes the medical treatment difficult. Caution must be taken to perform endoventriculoplasty in patients who are severely ill, especially those recently affected by myocardial infarction. When the clinical conditions dictate the operation, a nonenthusiastic volume reduction seems to be a prudent option. (J T HORAC C ARDIOVASC S URG 1995;109:694-701)

Clinical relevance of Doppler pulmonary venous flow characteristics in constrictive pericarditis.

The purpose of this study was to determine the diagnostic value of Doppler pulmonary venous flow in constrictive pericarditis, as assessed by transoesophageal echocardiography. It has been demonstrated previously that increased respiratory variation in Doppler pulmonary venous, but not in transmitral flow velocities, can identify patients with constrictive pericarditis, when transoesophageal echocardiography is used. In the present study we compared a group of 10 patients with constrictive pericarditis and a control group of 15 normal subjects with respect to pulmonary venous and transmitral flow velocities and their respiratory variation. Peak velocities and velocity time integrals of the systolic, early diastolic and late diastolic reversed pulmonary venous flow waves were measured. Peak velocities and velocity time integrals of the early and late diastolic transmitral flow waves were also measured. Measurements were made irrespective of the respiratory cycle, at the onset of inspiration and at the onset of expiration. Values for inspiration and expiration were expressed as percent difference of those obtained irrespective of the respiratory cycle. Peak velocity and velocity time integral of the pulmonary venous systolic and diastolic waves were significantly lower than in normal subjects. Furthermore, the difference between peak velocities of the diastolic wave obtained at the onset of inspiration and obtained irrespective of the respiratory cycle was significantly larger in constrictive pericarditis than in the control group (-20% vs -9%, P < 0.05). This also applied to the difference between velocity time integrals of the diastolic wave obtained at the onset of inspiration and obtained irrespective of the respiratory cycle (-22% vs -12%, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Differential effects of dobutamine and a phosphodiesterase inhibitor on early diastolic filling in patients with congestive heart failure

Objectives. This study was designed to compare the influence of beta-adrenergic stimulation (dobutamine) and a selective phosphodiesterase inhibitor (MS-857) on left ventricular diastolic performance and Doppler transmitral flow velocity patterns in patients with congestive heart failure and to elucidate the mechanisms for changes in early diastolic filling induced by each agent.Background. Both beta-adrenergic agonists and phosphodiesterase inhibitors act through the cyclic adenosine monophosphate pathway. However, it is controversial whether they have similar effects on diastolic performance. No previous studies have investigated the effects of these agents on Doppler-derived measurements of diastolic filling. We hypothesized that they would have different effects on early diastolic filling in patients with congestive heart failure.Methods. Twenty patients with chronic congestive heart failure resulting from idiopathic dilated cardiomyopathy were randomized to receive intravenous infusion of dobutamine (5 μg/kg body weight per min, n = 10) or oral administration of MS-857 (15 mg, n = 10). Transmitral flow velocity patterns were obtained with simultaneous recordings of pressure-volume loops using a conductance catheter with a micromanometer tip before and after drug administration.Results. Left ventricular filling pressure was reduced by both agents. Dobutamine decreased the time constant of isovolumetric relaxation and increased the difference between pulmonary artery wedge pressure at the peak of the vwave and left ventricular minimal pressure (10 ± 3 to 12 ± 4 mm Hg, p < 0.01) and peak early filling velocity (47 ± 7 to 56 ± 11 cm/s, p < 0.01). The diastolic pressure-volume relation showed a leftward shift in all patients. In contrast, MS-857 did not affect the time constant but maintained the pressure difference (9 ± 3 to 8 ± 3 mm Hg, p = NS) and peak early filling velocity (50 ± 7 to 49 ± 12 cm/s, p = NS). The diastolic pressure-volume relation after MS-857 showed a downward shift in most patients.Conclusions. These results indicate that beta-adrenergic stimulation and phosphodiesterase inhibitors have different effects on early diastolic filling through different mechanisms in patients with congestive heart failure.

Suppression of left ventricular early diastolic filling by long axis asynchrony.

To assess how early diastolic transmitral flow is suppressed in a group of patients in whom effective ventricular filling occurred exclusively with atrial systole. Prospective examination of the left ventricular transverse and longitudinal axes and transmitral Doppler flow. A tertiary referral centre for cardiac diseases. 20 patients (mean (SD) age 65 (10) years) with isolated transmitral late diastolic flow were studied. None had sinus tachycardia, prolonged PR interval or a summation flow pattern. 21 normal individuals of similar age served as controls. The left ventricle was usually dilated, end diastolic diameter (6.6 (1.0) v 4.9 (0.5) cm, P < 0.001) and end systolic diameter (5.4 (1.1) v 3.3 (0.5) cm, P < 0.001) were both increased, and fractional shortening of the minor axis reduced (16 (7)% v 30 (10)%, P < 0.001) in patients in whom left ventricular early diastolic filling was absent compared with those of normal controls. Mitral valve opening was late after aortic valve closure (A2) (115 (30) v 60 (10) ms, P < 0.001). The minor axis increased during this period (30 (20)% v 8.6 (2.5)%, P < 0.001). Onset of detectable transmitral flow was further delayed after cusp separation (85 (25) v 25 (10) ms, P < 0.001). Left ventricular long axis function was very abnormal. Onset of shortening was delayed with respect to the q wave at the left and septal sites (150 (40) v 90 (20) ms and 145 (30) v 80 (10) ms respectively, P < 0.001) and major shortening occurred after, rather than before, A2 (25 (12) v -10 (2.5)% and 50 (30) v -6.6 (0.3)% total excursion, P < 0.001). Although the long axis lengthened a little at the start of early diastole, its dominant component occurred in late diastole to coincide with atrial systole. The relative A wave was thus greatly increased at both sites (67 (17) v 29 (6)% and 77 (13) v 33 (8)%, P < 0.001). Prolonged left ventricular long axis shortening and delayed onset of lengthening effectively suppress early diastolic transmitral flow even though the minor axis increases and mitral cusps separate apparently normally. This grossly asynchronous left ventricular relaxation may interfere with filling by dissipating normal ventricular restoring forces.

Doppler evaluation of left ventricular diastolic filling in Behçet's disease

Although cardiac involvement such as pericarditis, myocarditis, coronary arteritis and valvular disease in Behçet's disease occurs, few studies have assessed left ventricular diastolic function. This study assesses the prevalence of both systolic and diastolic left ventricular dysfunction in patients with Behçet's disease who have no clinical cardiac manifestations. Twenty-two patients (12 women and 10 men, mean age 34 ± 2.4 years) underwent full clinical examination, electrocardiography, M-mode, two-dimensional, and Doppler echocardiography. The mean disease duration was 5 ± 4.7 years (range, 1 month-16 years). An age and sex-matched control group of 20 healthy subjects was also studied. Prolonged isovolumic relaxation time, prolonged deceleration time, reversal of the early and late peak transmitral diastolic flow velocities, late peak transmitral diastolic flow velocities ( E A ratio) and increased atrial filling fraction were noted in five patients. It is concluded that left ventricular dysfunction occurs frequently in patients with Behçet's disease and Doppler echocardiography may be valuable in detecting diastolic filling abnormalities as an early sign of cardiac involvement.

Doppler Diastolic Transmitral Flow Patterns in Severe Heart Failure: Response to Controlled Changes in Filling Pressure Using Intravenous Isosorbide Dinitrate

Serial Doppler diastolic transmitral flow patterns were compared with simultaneous hemodynamic measurements in a homogeneous group of patients with severe (New York Heart Association class 4) heart failure who were receiving high dose (508 +/- 271 micrograms/min) intravenous isosorbide dinitrate. The Doppler tracing uniformly showed a severe restrictive pattern, with tall peak early diastolic filling (E) wave (84 +/- 12 cm/s), small late filling (A) wave (28 +/- 8 cm/s) and very high E/A ratio (3.2 +/- 0.8). Isosorbide dinitrate decreased wedge pressure and systemic vascular resistance by a third and increased cardiac index by more than 40%. Transmitral Doppler E/A ratio changed directly in relation to the changes in pulmonary capillary wedge (r = 0.85, p = 0.03) and right atrial pressure (r = 0.84, p = 0.03), indicating preload dependence of transmitral flow velocity, even in severe heart failure.

Timing of recipient atrial contraction: A major determinant of transmitral diastolic flow in orthotopic cardiac transplantation

The effect of recipient left atrial contraction on diastolic transmitral flow was studied in eight asymptomatic heart transplant patients (seven men and one woman, mean age 51.8 ± 9.7 years) with normal left ventricular systolic function. The transmitral flow velocity profile was evaluated in 326 beats (mean 40.8 ± 12 beats, range 20 to 58 beats/patient). Recipient left atrial contraction was classified as early diastolic, late diastolic, and systolic. Results showed: (1) early diastolic transmitral flow velocity integral (in centimeters) was lower ( p < 0.05) following late diastolic recipient left atrial contractions (7.5 ± 2.1) compared with early diastolic (10.1 ± 2.7) or systolic (8.5 ± 1.5) recipient left atrial contractions; (2) late diastolic transmitral flow velocity integral was higher following late diastolic (4.7 ± 1.8) compared with systolic (4.1 ± 1.9) recipient left atrial contractions and was virtually abolished (0.45 ± 14) following early diastolic recipient left atrial contractions; and (3) total diastolic transmitral flow velocity integral was significantly higher ( p < 0.05) following late diastolic and systolic (12.2 ± 2.8 and 12.0 ± 2.5) compared with early diastolic left atrial contractions (10.5 ± 2.8). Thus recipient left atrial contraction is a significant determinant of the transmitral diastolic flow pattern in heart transplant patients. Variations in the timing of recipient left atrial contraction may lead to fluctuations of diastolic flow and may compromise cardiac output.

Aortic distensibility and left ventricular structure and function in isolated systolic hypertension

Aortic mechanical properties were assessed in a group of elderly subjects with untreated isolated systolic hypertension using two-dimensional echocardiography. Echocardiographic (two-dimensional and Doppler) assessment of left ventricular structure and function was also made. Ten subjects (mean age 71.7 +/- 1.9 years, 20% male, mean clinic blood pressure 163.6/79.2 +/- 1.2/2.0 mmHg) were compared with 16 normotensive subjects of similar age (69.4 +/- 1.6 years, 38% male, mean clinic blood pressure 129.8/78.2 +/- 3.2/2.9 mmHg). Aortic distensibility at the level of the transverse aortic arch was significantly reduced among subjects with isolated systolic hypertension. The thickness of the interventricular septum was approximately 20% greater in the hypertensive subjects (P < 0.01) and the average wall thickness to radius ratio was increased by 30%. Patterns of transmitral diastolic flow were also different in subjects with isolated systolic hypertension. Deceleration time was significantly greater (P < 0.01) and the ratio of early to late transmitral diastolic peak flow velocities was significantly less in the hypertensive (P < 0.05) than in the normotensive group. Left ventricular systolic function was well preserved. These findings are consistent with the suggestion that isolated systolic hypertension represents a state of increased aortic stiffness which may contribute to the development of left ventricular hypertrophy. Whether this increase in aortic stiffness is the cause or effect of the elevated systolic blood pressure remains unresolved.

Left ventricular systolic and diastolic function, and exercise capacity six to eight weeks after acute myocardial infarction

Echocardiographic and Doppler-derived measurements of left ventricular (LV) function at rest were examined as predictors of maximal bicycle exercise capacity in a homogeneous group of 115 patients with mild to moderate LV dysfunction (ejection fraction 22 to 56%, median 43%) participating in the DEFIANT study of nisoldipine after acute myocardial infarction. Although the relations were not exact, peak exercise work load 7 weeks after infarction correlated with measurements of diastolic LV function at rest. Exercise work load was inversely related to peak late diastolic transmitral blood flow velocity (A wave) (slope −86.6; 95% confidence interval −120.9 to −52.2) and directly to the E/A ratio (slope 20.5; 95% confidence interval 6.0 to 35.1). The relations between exercise work load and peak late diastolic flow velocity remained significant after correction for age, sex, heart rate at rest, and use of β-blocking drugs or nisoldipine. There was no relation between peak exercise work load and peak early diastolic transmitral flow velocity (E wave), isovolumic relaxation period or deceleration time. Measurements of systolic LV function (LV enddiastolic and end-systolic volumes, and ejection fraction, stroke volume and cardiac index) were also not significant as predictors of exercise capacity.

Influence of pericardium on left atrial compliance and pulmonary venous flow.

We studied seven open-chest anesthetized dogs to test the hypothesis that left atrial (LA) compliance is increased after pericardiectomy and to determine the effect of pericardiectomy on left atrial reservoir and conduit function. Two orthogonal sonomicrometer crystal pairs were used to estimate LA volume, and LA filling was assessed with a pulmonary vein (PV) flow probe. The left ventricular (LV) systolic (JFTI) and diastolic (KFTI) PV flow integrals were used as indexes of LA reservoir and conduit function, respectively. Diastolic LV transmitral flow was assessed with transesophageal Doppler echocardiography. Data were acquired over a wide range of intracardiac pressures and volumes obtained by intravenous hetastarch infusion both before and after pericardiectomy. The mean dynamic stiffness constant of the LA diastolic pressure-volume relation was significantly greater before pericardiectomy than afterwards (0.15 +/- 0.04 vs. 0.08 +/- 0.03 ml-1, P < 0.05). Data were analyzed before and after pericardiectomy at three matched levels of left atrial pressure (LAP; 7, 13, and 20 mmHg). The J-to-KFTI ratio increased significantly with volume infusion and was significantly less after pericardiectomy than before (1.2 +/- 0.7 vs. 1.2 +/- 0.6, 1.8 +/- 0.6 vs. 2.2 +/- 0.9, and 2.0 +/- 0.8 vs. 2.6 +/- 0.9 at low, mid, and high levels of LAP, respectively; P < 0.05 at mid and high levels of LAP). Peak early transmitral velocity increased with both volume infusion and pericardiectomy. We conclude that pericardiectomy increases LA compliance and early LV filling rate and is accompanied by a relatively greater augmentation in conduit than reservoir function of the left atrium.

Doppler echocardiographic evidence of left ventricular diastolic dysfunction in ankylosing spondylitis

Although cardiac involvement in the form of conduction abnormalities or aortic regurgitation occurs in 5 to 10% of patients with ankylosing spondylitis, few studies have assessed left ventricular (LV) function. This study assesses the prevalence of both systolic and diastolic LV dysfunction and other cardiac abnormalities in patients with ankylosing spondylitis who have no clinical cardiac manifestations. Fifty-nine patients (49 men and 10 women, mean age 42 ± 10 years) underwent full clinical examination, electrocardiography, 24-hour Holter monitoring and 2-dimensional, M-mode and Doppler echocardiography. Mean disease duration was 17 ± 9 years (range 1 to 42). Seventeen patients had evidence of noncardiac extraarticular manifestations. Precordial examination was normal in all. An age- and sex-matched control group of 44 healthy subjects was also studied. On echocardiography, abnormal LV diastolic function was detected in 12 patients (20%). Prolonged isovolumic relaxation time, prolonged deceleration time, reduced rate of descent of flow velocity in early diastole (EF slope) and reversal of the early and late peak transmitral diastolic flow velocities ( E A ratio) were noted in 9 patients. In 3 patients there was an increased E A ratio, reduced deceleration time and increased EF slope. Mild aortic regurgitation and mitral regurgitation was seen in 1 and 3 patients, respectively. No abnormalities of left atrial size, LV systolic or diastolic dimensions or wall thicknesses were noted. There was no correlation between the presence of LV diastolic dysfunction and age, disease severity, disease duration, or the presence of extraarticular manifestations. It is concluded that LV diastolic dysfunction occurs frequently in patients with ankylosing spondylitis, even in the absence of clinical cardiac involvement.

Delayed restoration of atrial function after conversion of atrial flutter by pacing or electrical cardioversion

It is often suggested but never proven that atrial function is not affected during atrial flutter, nor after its conversion to normal sinus rhythm. To evaluate this hypothesis, a prospective study was performed in 22 patients (age range 20 to 88 years) with atrial flutter. Diastolic transmitral flow was analyzed with echo-Doppler before and after conversion. After randomization, conversion was attempted with overdrive pacing or up to two 50 J shocks. If the initial method was unsuccessful, a 200 J shock was administered. All patients were converted to sinus rhythm with this protocol. Shortly after conversion (at 1 and 6 hours), atrial contribution to ventricular filling was absent in 4 of 22 patients. In the remaining 18 patients, atrial contribution to ventricular filling was small. Atrial contribution to transmitral flow improved from 20 to 27% within 24 hours (p < 0.01) and increased further to 38% at 6 weeks (p < 0.005). Peak velocity of late diastolic filling increased from 0.28 m/s after 1 hour to 0.39 m/s after 24 hours (p < 0.0001) and improved even further during later follow-up. In 1 patient, an effective atrial systole was not observed until the 14th day. Cardiac output did not change significantly during the study period. No differences were observed between the conversion modalities. In conclusion, atrial dysfunction is present immediately after conversion of atrial flutter to normal sinus rhythm. This dysfunction occurs also after overdrive pacing and can last >1 week. The findings suggest that stasis in the atria can remain temporarily present after successful conversion of atrial flutter to sinus rhythm.

The Rate of Left Atrial Pressure Drop Affects Early Diastolic Transmitral Flow Velocity Patterns

The Rate of Left Atrial Pressure Drop Affects Early Diastolic Transmitral Flow Velocity Patterns

Ventricular Function in Snorers and Patients with Obstructive Sleep Apnea

We hypothesized that intermittent hypoxemia and increased ventricular afterload due to obstructive apnea during sleep (OSA) would cause chronic left ventricular dysfunction. Overnight polysomnography, M-mode and two-dimensional echo-Doppler studies while awake were performed on 51 consecutive snorers, 30 with OSA and 21 without apnea. Patients with previous myocardial infarction, awake hypoxemia or hypercapnia, or other causes of nocturnal hypoxemia were excluded. Echo-Doppler measurements included end-diastolic right and left ventricular dimensions and wall thickness, indices of left ventricular systolic performance (fractional shortening, ejection fraction and ejection time and diastolic performance, (isovolumic relaxation time, ratio of peak early [E] to late [A] diastolic transmitral flow and mitral pressure half-time). Both OSA patients and nonapneic snorers were of similar age. Although OSA patients were heavier, had a greater apnea-hypopnea index, and significant nocturnal hypoxemia, their echo-Doppler measurements were within normal limits and were not significantly different from nonapneic snorers. It is concluded that isolated obstructive sleep apnea does not cause chronic left ventricular dysfunction.

Relationship between angiographic infarct size and left ventricular filling

Infarct size may influence left ventricular filling after acute myocardial infarction. Pulsed Doppler transmitral flow velocities were compared in 47 patients at 7 ± 6 days following acute myocardial infarction and 47 age-matched controls. Patients were stratified by angiographic infarct size into Groups I, II, III (corresponding angiographic hypokinetic scores < 2; 2–2.99; ≥ 3 SD/cord). Early diastolic transmitral Doppler flow velocities did not differ between infarct groups but atrial transmitral Doppler flow measurements did: peak A velocity ( p = 0.001), A velocity time integral ( p < 0.001), and total velocity time integral ( p = 0.001). Compared to controls atrial transmitral Doppler flow was augmented in Group I, whilst atrial and total transmitral Doppler flow were depressed in Group III. Peak A velocity and A velocity time integral were inversely related to infarct size ( R = −0.44 to −0.54) and directly to left ventricular ejection fraction ( R = 0.59 to 0.65). Large infarct size following myocardial infarction is associated with lower atrial and total transmitral Doppler flow velocities.