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PubMed2005

Multicenter, prospective, randomized safety and efficacy study of a new atrial-based managed ventricular pacing mode (MVP) in dual chamber ICDs.

BACKGROUND: Ventricular desynchronization caused by right ventricular pacing may impair ventricular function and increase risk of heart failure (CHF), atrial fibrillation (AF), and death. Conventional DDD/R mode often results in high cumulative percentage ventricular pacing (Cum%VP). We hypothesized that a new managed ventricular pacing mode (MVP) would safely provide AAI/R pacing with ventricular monitoring and DDD/R during AV block (AVB) and reduce Cum%VP compared to DDD/R. METHODS: MVP RAMware was downloaded in 181 patients with Marquis DR ICDs. Patients were initially randomized to either MVP or DDD/R for 1 month, then crossed over to the opposite mode for 1 month. ICD diagnostics were analyzed for cumulative percentage atrial pacing (Cum%AP), Cum%VP, and duration of DDD/R pacing for spontaneous AVB. RESULTS: Baseline characteristics included age 66 +/- 12 years, EF 36 +/- 14%, and NYHA Class II-III 36%. Baseline PR interval was 190 +/- 53 msec and programmed AV intervals (DDD/R) were 216 +/- 50 (paced)/189 +/- 53 (sensed) msec. Mean Cum%VP was significantly lower in MVP versus DDD/R (4.1 +/- 16.3 vs 73.8 +/- 32.5, P < 0.0001). The median absolute and relative reductions in Cum%VP during MVP were 85.0 and 99.9, respectively. Mean Cum%AP was not different between MVP versus DDD/R (48.7 +/- 38.5 vs 47.3 +/- 38.4, P = 0.83). During MVP overall time spent in AAI/R was 89.6% (intrinsic conduction), DDD/R 6.7% (intermittent AVB), and DDI/R 3.7% (AF). No adverse events were attributed to MVP. CONCLUSIONS: MVP safely achieves functional atrial pacing by limiting ventricular pacing to periods of intermittent AVB and AF in ICD patients, significantly reducing Cum%VP compared to DDD/R. MVP is a universal pacing mode that adapts to AVB and AF, providing both atrial pacing and ventricular pacing support when needed.

Adult↗
PubMed1985

Electrophysiology of functional subsidiary pacemakers in canine right atrium.

Glass microelectrodes were used to study the electrical activity of the subsidiary atrial pacemaker (SAP) cells that maintain atrial excitation after suppression of the sinoatrial node. Tissues with documented SAP activity were isolated from the canine inferior right atrium and superfused in vitro with Tyrode solution containing norepinephrine (NE, 10(-8)-10(-7) M). SAP action potentials exhibited prominent diastolic depolarization and a significantly lower maximum diastolic potential, take-off potential, overshoot, rate of rise, and amplitude than typical atrial muscle. Withdrawal of NE completely blocked SAP propagation, although SAP automaticity continued at a slower rate. Acetylcholine (ACh, 5 X 10(-8) M) usually produced complete exit block and decreased spontaneous rate. Higher concentrations of ACh (10(-6) M) elicited a prominent hyperpolarization (19.2 +/- 6.6 mV), completely suppressing SAP automaticity. In quiescent preparations exposed to NE greater than or equal to 10(-7) M, external stimuli at short cycle lengths (less than 1,000 ms) elicited action potentials with delayed afterdepolarizations, which frequently caused nondriven repetitive activity. This triggered activity was inhibited by verapamil or withdrawal of NE. These studies identify and characterize the electrical activity of functional subsidiary pacemakers located in a specific region of the inferior right atrium. In addition, fibers within this region display triggered activity. Spontaneous activity generated by fibers within the SAP region may cause atrial dysrhythmias.

Acetylcholine↗
PubMed1995

A case of right atrial myxoma--effect of large myxoma in the right atrium studied by M-mode and Doppler echocardiography.

Doppler profiles are rarely used to assess cardiac function that has been partially impaired by a sizeable myxoma in the right atrium or to evaluate the improvement caused by extirpation of the tumor. In a 54-year-old man with a large right atrial myxoma (6.5 x 5.5 x 4.0 cm) along with first-degree atrioventricular (AV) block, M-mode and pulsed Doppler echocardiography were used to evaluate the left ventricular systolic and diastolic function before and 1 month after surgical removal of the myxoma. End-diastolic left ventricular (LV) and left atrial diameters increased postsurgically from 47 to 51 mm and from 38 to 41 mm, respectively, while end-systolic LV remained unchanged. In the LV inflow pattern, peak early filling velocity (E) increased substantially (preoperative 31, postoperative 58 cm/sec), with no change in peak late filling velocity (A) (53 cm/sec), which gave a favorable E/A ratio (from 0.58 to 1.09). First-degree AV block resolved after tumor resection (PR interval: 0.23 vs 0.20 sec). Improved LV diastolic function associated with natural recovery from the myxoma was ascribed to the restoration of preload and recovery of systolic function. The results of this study show that removal of a large myxoma in the right atrium is important not only for preventing possible obstruction of the tricuspid orifice, eliminating pulmonary emboli, and maintaining systolic function, but also for restoring LV diastolic function.

Diastole↗
PubMedDate not supplied

[Left atrial function during left ventricular diastole evaluated by left atrial angiography and left ventriculography].

The left atrium (LA) stores part of the right ventricular stroke volume during ventricular systole for passive release into the left ventricle (LV) during ventricular early diastole and active release during ventricular late diastole (passive and active contraction). The rest of the right ventricular stroke volume flows through the LA from the pulmonary vascular bed to the LV (LA conduit function). The factors affecting these LA functions were evaluated during ventricular diastole by left atrial angiography and left ventriculography in 21 patients with normal LV ejection fraction (0.53-0.76), but without coronary artery disease and valvular heart disease, aged 40-70 years. LV stroke volume was calculated from left ventriculograms. The maximal LA volume, minimal LA volume, and LA volume at the beginning of the left atrial active contraction were calculated from the left atrial angiograms, and further corrected by a regression equation (true volume = 0.91 x calculated volume -1.1). The LA reservoir volume, LA passive contraction volume, LA active contraction volume, and LA conduit volume were obtained. LA conduit volume correlated significantly with LV stroke volume (r = 0.97), but not with maximal LA volume and LA reservoir volume. LA active contraction volume correlated significantly with LA reservoir volume, LA volume at the beginning of LA active contraction, and maximal LA volume (r = 0.85, 0.60, 0.54, respectively). LA passive contraction volume did not correlate with any factor, and was grossly independent of LV stroke volume. LA conduit volume may be associated with LV diastolic function, and LA active contraction volume appears to increase with increased LA volume.

Adult↗
PubMed1994

Reduction of beta-adrenergic receptors in atrial cell membranes of patients following mild to moderate heart failure.

The density of cardiac beta-adrenoceptors (Bmax) was measured in eighteen patients [2 with atrial septal defect (ostium secundum), 4 with aortic valve disease, 3 with mitral valve disease, 1 with aortic and mitral valve disease, 5 with a history of myocardial infarction, and 3 with angina pectoris] following mild to moderate cardiac failure. Measures were obtained by cardiac catheterization prior to cardiac surgery and also during the surgical procedures. On the basis of symptoms immediately preceding surgery, the severity of the condition in each patient was categorized as either Class I (n = 5) or Class II (n = 13) following the New York Heart Association (NYHA) functional classification system. The Bmax was measured using right atrial appendage tissue obtained during cardiac surgery. [125I]-iodocyanopindolol was used for the assay. The Bmax of atrial cell membranes in patients with NYHA class II was significantly lower than that of class I (34.1 +/- 2.5 vs 55.4 +/- 9.3 fmol/mg protein, M +/- SE, p < 0.05). Correlation coefficients between the Bmax and hemodynamic parameters measured just prior to cardiac surgery were examined, but only that between Bmax and the minimum value of the time derivative of left ventricular pressure (max negative dp/dt) was significant (r = -0.552, p < 0.05). Further study is needed to understand and clarify the relationship between Bmax and dp/dt min.

Adult↗
PubMed1992

Electrophysiological effect of the maze procedure on canine sinoatrial node function.

The maze procedure is an operation that has had great initial success in curing atrial fibrillation. This procedure includes several right atrial incisions that may interrupt the integrity of the sinoatrial node or its arterial supply. To assess the effect of the maze procedure on sinus node function (SNF), the following studies were performed: sinus node recovery times (SNRT), corrected SNRT (CSNRT), CSNRT under autonomic blockade maximal heart rate and intrinsic heart rates. Thirty-four dogs underwent a right thoracotomy with cardiopulmonary bypass (CPB). The dogs were divided into three groups. Group 1 (n = 9), the sham group, underwent CPB without any incisions. Group 2 (n = 8) underwent CPB and one of the right atrial incisions. Group 3 (n = 18) underwent CPB and all three of the right atrial incisions. SNF was determined before and after the procedure. Groups 1 and 2 had no significant difference in measured SNF acutely after the procedure. In Group 3 the mean SNRT increased from 552 msec to 1,984 msec (P = 0.005). Sinus node dysfunction was corroborated by all studies. In the chronic studies, a trend toward recovery of SNF was observed. The maze procedure results in significant acute sinus node dysfunction. This dysfunction may resolve spontaneously over the ensuing months. Modifications of the maze procedure that avoid the sinus node or its blood supply area may reduce procedure related sinus node dysfunction.

Animals↗
PubMed1981

Cardiac function in chronic bronchitis: effects of pacing and plasma expansion.

1. We have investigated left ventricular function in 25 selected patients with chronic bronchitis by use of atrial pacing and plasma volume expansion. Nine subjects had a past history of acute respiratory failure. None had either clinical or electrocardiographic signs of coronary heart disease. Paradoxical pulse was absent, since the difference between the highest and lowest systolic arterial pressure throughout the respiratory cycle was 5.4 +/- 1.5 mmHg. 2. During atrial pacing, at a mean rate of 145 +/- 15, about 80% of the predicted maximal rate, none of the patients showed anginal pain or ventricular repolarization abnormality. Cardiac output remained unchanged compared with control values. 3. Plasma volume expansion was achieved by intravenous injection of 1 litre of gelatin over 30 min. Cardiac output, pulmonary wedge pressure and right atrial pressure rose as reported in literature for normal subjects. In four patients cardiac output did not increase although wedge pressure and right atrial pressure did; two of these four patients also had an overshoot in pulmonary wedge pressure just after atrial pacing, suggesting left ventricular dysfunction. Three out of 25 patients had high control right atrial pressures, probably in relation to impaired right ventricular function. No paradoxical pulse occurred during plasma volume expansion. Therefore competition for space in the pericardium between ventricles was unlikely. 4. Our data suggest that left ventricular dysfunction is rare in patients with chronic obstructive pulmonary disease. There was no significant difference between subjects with and without a past history of acute respiratory failure.

Adult↗
PubMed2002

Doppler echocardiographic evaluation of right ventricular diastolic function in hypertrophic cardiomyopathy.

AIMS: Left ventricular diastolic function in patients with hypertrophic cardiomyopathy has been adequately studied. In contrast there are few studies concerning right ventricular diastolic function in hypertrophic cardiomyopathy. We studied right ventricular diastolic function in patients with hypertrophic cardiomyopathy using Doppler echocardiography. METHODS AND RESULTS: We studied 20 patients with hypertrophic cardiomyopathy (mean age 43.6+/-13.8 years) and 20 healthy volunteers (control group, mean age 43+/-13.8 years). We calculated left ventricular and right ventricular diastolic indices using pulsed Doppler echocardiography. Hypertrophic cardiomyopathy patients compared with controls had significantly lower right ventricular-E/A ratio (1.01+/-0.40 vs 1.30+/-0.28, P<0.04), significantly prolonged right ventricular isovolumic relaxation time (170+/-72 vs 32+/-23 ms, P<0.001), and also significantly prolonged right ventricular deceleration time (160+/-58 vs 118+/-35 ms, P<0.01). There was also strong significant correlation between right ventricular deceleration time and left ventricular deceleration time (r=0.78), right ventricular-E/A ratio and left atrial filling fraction (r=-0.55) and between right atrial filling fraction and left atrial filling fraction (r=0.75). CONCLUSIONS: Right ventricular diastolic function in patients with hypertrophic cardiomyopathy is impaired, reflecting abnormal relaxation. Right ventricular diastolic indices correlate well with those of left ventricle.

Adolescent↗
PubMed1998

"Stunning" of the left atrium after spontaneous conversion of atrial fibrillation to sinus rhythm: demonstration by transesophageal Doppler techniques in a canine model.

OBJECTIVES: This study compared left atrial and left atrial appendage contraction velocities in sinus rhythm before and after a brief period of atrial fibrillation in a canine model. BACKGROUND: In patients, left atrial appendage contraction velocities measured during sinus rhythm after cardioversion from atrial fibrillation are depressed relative to left atrial appendage emptying velocities measured during atrial fibrillation, suggesting that the left atrial appendage is mechanically "stunned." METHODS: This phenomenon was studied in a canine model of acute (60 min) pacing-induced atrial fibrillation followed by spontaneous reversion to sinus rhythm using epicardial and transesophageal pulsed wave Doppler. Unique features of the model include: 1) comparison of left atrial function postconversion to baseline sinus rhythm rather than to measurements during atrial fibrillation, 2) control of the duration of atrial fibrillation and 3) elimination of the extraneous influences of direct current shock and antiarrhythmic agents, which may independently depress left atrial function. RESULTS: Hemodynamic conditions (heart rate, mean arterial pressure, cardiac output, mean pulmonary artery pressure, mean right atrial pressure and mean left atrial pressure) at baseline, during 60 min of atrial fibrillation and after reversion to sinus rhythm were constant throughout the study period. Peak left atrial contraction velocities (measured from the transmitral flow velocity profile) were significantly (p < 0.02) reduced to 64+/-22% of baseline values upon spontaneous conversion of atrial fibrillation to sinus rhythm and recovered to basal values by 20 min after resumption of sinus rhythm. Peak left atrial appendage contraction velocities were significantly (p < 0.001) reduced to 49+/-24% of baseline values upon spontaneous conversion of atrial fibrillation to sinus rhythm and recovered to basal values by 40 min after reversion to sinus rhythm. CONCLUSIONS: Even brief (60 min) periods of atrial fibrillation in normal canine hearts result in marked depression of global left atrial systolic function and regional left atrial (left atrial appendage) systolic function upon resumption of sinus rhythm. This "mechanical stunning" of left atrial systolic function appears to be more profound and of longer duration for the left atrial appendage compared with the left atrium as a whole, which may predispose the appendage to blood stasis and thrombus formation. Chronic models of atrial fibrillation need to be developed to examine the impact of longer periods of atrial fibrillation upon the magnitude and duration of postconversion left atrial "stunning."

Animals↗
PubMed1991

Influence of endothelin on cardiovascular function, oxygen free radicals, and blood chemistry.

Endothelin, a peptide that is derived from vascular endothelial cells, is a potent constrictor of mammalian blood vessels in in vitro studies. Various clinical conditions have been reported to be associated with an increase in the blood and tissue levels of endothelin. In the present study, the effects of two doses (2.059 and 4.118 micrograms/kg, intravenously) of endothelin on cardiac function and contractility; blood lactate, gases, and pH levels; blood and cardiac tissue MDA levels; PMN leukocyte chemiluminescence activity; and total WBC and PMN leukocyte counts were investigated in anesthetized dogs. Hemodynamic measurements and collection of blood samples for various biochemical measurements were made before and at various intervals up to 2 hours after endothelin administration. Endothelin in the large dose (4.118 micrograms/kg) produced a prolonged decrease in the indices of cardiac contractility and cardiac function and increases in TSVR, PVR, and mean right atrial pressure. The changes in the hemodynamic parameters with the smaller dose (2.059 micrograms/kg) were similar but of smaller magnitude. Significant decreases in dp/dt at CPIP:PAW and CI and increases in TSVR and PVR were observed with the smaller dose of endothelin. There were decreases in the blood HCO3- and pH levels and an increase in H+ and blood lactate concentration and CK activity with the high dose of endothelin. No changes were observed in blood PO2 and PCO2 with either dose of endothelin. Circulating WBCs and PMN leukocytes decreased significantly with both doses of endothelin. There were no changes in the oxygen free radical-producing activity of PMN leukocytes and in the blood and cardiac tissue MDA levels. These results suggest that endothelin decreased cardiac function and cardiac contractility and increased SVR and PVR. The decrease in cardiac function and contractility may be due to ischemia from constriction of coronary arteries. The hemodynamic changes are unlikely be due to oxygen free radicals since there was no increase in the blood and cardiac tissue MDA levels and no change in the PMN chemiluminescence. These studies suggest that increases in endothelin levels in certain clinical conditions might cause added deleterious effects on cardiovascular function.

Animals↗
PubMed2007

Atrial tachycardia arising from the right atrial inferoseptum masquerading as common atrial flutter.

Radiofrequency catheter ablation was performed in 2 patients with atrial tachycardia (AT). In both cases the AT originated from the inferoseptal portion of the right atrium, and the cycle length was 210 ms. The surface ECG demonstrated common counterclockwise atrial flutter, probably caused by functional block in the clockwise direction at the cavo-tricuspid isthmus and posterior right atrium with rapid activation of the origin. Although rare (2%), AT originating from the inferoseptum of the right atrium should be considered when the surface ECG exhibits common atrial flutter.

Adult↗
PubMed1991

Evaluation of right ventricular function using gated equilibrium blood pool radionuclide ventriculography in patients with congenital volume and pressure overload late after surgical repair.

The effects of congenital right ventricular pressure and volume overload were studied in 3 patients with pulmonary stenosis, 7 with atrial septal defect and 6 with atrial septal defect plus pulmonary stenosis late after successful surgical correction. Gated equilibrium blood pool radionuclide ventriculography was used to measure right ventricular function at rest and during exercise and to compare it with eight normal subjects. Right ventricular ejection fractions at rest and during exercise were measured to be 61 +/- 9% and 66 +/- 13%, respectively, in the group with pulmonary stenosis, 49 +/- 7% and 54 +/- 8% in the group with atrial septal defect, and 65 +/- 13% and 69 +/- 13% in the group with atrial septal defect plus pulmonary stenosis. The values in the groups with pulmonary stenosis and atrial septal defect plus pulmonary stenosis were significantly higher than the control subjects (45 +/- 5% and 51 +/- 5%, p less than 0.01). The peak filling rate at rest and during exercise was also significantly higher in the groups with pulmonary stenosis and atrial septal defect plus pulmonary stenosis than in controls (at rest, 2.72 +/- 0.72, 2.53 +/- 0.94 vs. 1.64 +/- 0.24 p less than 0.05; during exercise, 4.38 +/- 1.23, 4.13 +/- 1.18 vs. 2.52 +/- 0.62, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1998

[Acute changes in wavelength of the process of auricular activation induced by stretching. Experimental study].

OBJECTIVE: An evaluation is made of the acute modifications in the wavelength of the atrial excitation process induced by atrial stretching. MATERIAL AND METHODS: In 10 isolated Langendorff-perfused rabbit hearts and using a multiple electrode the wavelength of the atrial activation process (functional refractory period x conduction velocity) was determined in the right atrium. An analysis was also made of the inducibility of rapid repetitive atrial responses after 20 episodes of atrial burst pacing. Measurements were made under control conditions, after inducing two degrees of atrial wall stretch (D1 and D2), and following the suppression of atrial dilatation. RESULTS: Under control conditions the wavelength was 72.6 +/- 7.7 mm (250 ms cycle) and 54.0 +/- 5.1 mm (100 ms cycle). In D1 (mean longitudinal increase in atrial wall length = 24 +/- 3%) the wavelength shortened, with values of 59.8 +/- 6.6 mm (250 ms cycle; p < 0.01) and 44.9 +/- 5.1 mm (100 ms cycle; p < 0.01). In D2 (mean longitudinal increase in atrial wall length = 41 +/- 4%) the wavelength also shortened significantly, with values of 41.6 +/- 2.5 mm (250 ms cycle; p < 0.01 vs control) and 29.6 +/- 2.1 mm (100 ms cycle; p < 0.01 vs control). After suppressing atrial dilatation the wavelength was 65.7 +/- 8.0 mm (250 ms cycle, NS vs control) and 47.9 +/- 5.5 mm (100 ms cycle; NS vs control). The inducibility of rapid repetitive atrial responses increased during dilatation (22 episodes with over 30 consecutive repetitive responses in D1 [p < 0.01], 50 episodes in D2 [p < 0.001] vs 5 episodes under control conditions), and diminished after suppressing atrial dilatation (0 episodes with over 30 consecutive repetitive responses; p < 0.05). CONCLUSIONS: In the experimental model used, acute atrial dilatation produced a shortening in refractoriness and a decrease in conduction velocity. Both effects shortened the wavelength of the atrial activation process, facilitating the induction of atrial arrhythmias. The effects observed reverted upon suppressing atrial dilatation.

Animals↗
PubMed1991

Results of the Fontan procedure for patients with univentricular heart.

One hundred twenty-four consecutive patients with univentricular heart undergoing the Fontan operation were reviewed. Patients with tricuspid atresia or biventricular heart with hypoplasia of one ventricle were excluded. Eighty-four patients had left ventricular morphology. Atrioventricular connection was double-inlet (n = 76), common (n = 29), absent left atrioventricular connection (n = 14), and absent right atrioventricular connection (n = 5). Actuarial survival was 77% (70% confidence limits, 73% to 81%) at 1 year, 66% (70% confidence limits, 60% to 72%) at 5 years, and 49% (70% confidence limits, 36% to 61%) at 10 years, indicating a continuing risk for premature death. Multivariate analysis identified preoperative ventricular function and hypertrophy as risk factors for survival. High postrepair right atrial pressure (greater than 15 mm Hg) emerged as a strong intraoperative predictor of survival. Logistic regression analysis of these factors predicts high probability of death for certain subgroups of patients after the Fontan operation. Forty-four percent (n = 53) of these original 124 patients are alive and in New York Heart Association class I at follow-up. Thirty-eight percent (n = 33) of survivors have worse ventricular function than preoperative. Long-term survival is disappointing. Certain identifiable subgroups of patients with univentricular heart have unacceptable risks for the Fontan operation and should have alternate management. High postrepair right atrial pressure is an ominous sign, and if it persists the Fontan should be fenestrated or taken down.

Adolescent↗
PubMed1991

Survival in patients with primary pulmonary hypertension. Results from a national prospective registry.

OBJECTIVE: To characterize mortality in persons diagnosed with primary pulmonary hypertension and to investigate factors associated with survival. DESIGN: Registry with prospective follow-up. SETTING: Thirty-two clinical centers in the United States participating in the Patient Registry for the Characterization of Primary Pulmonary Hypertension supported by the National Heart, Lung, and Blood Institute. PATIENTS: Patients (194) diagnosed at clinical centers between 1 July 1981 and 31 December 1985 and followed through 8 August 1988. MEASUREMENTS: At diagnosis, measurements of hemodynamic variables, pulmonary function, and gas exchange variables were taken in addition to information on demographic variables, medical history, and life-style. Patients were followed for survival at 6-month intervals. MAIN RESULTS: The estimated median survival of these patients was 2.8 years (95% Cl, 1.9 to 3.7 years). Estimated single-year survival rates were as follows: at 1 year, 68% (Cl, 61% to 75%); at 3 years, 48% (Cl, 41% to 55%); and at 5 years, 34% (Cl, 24% to 44%). Variables associated with poor survival included a New York Heart Association (NYHA) functional class of III or IV, presence of Raynaud phenomenon, elevated mean right atrial pressure, elevated mean pulmonary artery pressure, decreased cardiac index, and decreased diffusing capacity for carbon monoxide (DLCO). Drug therapy at entry or discharge was not associated with survival duration. CONCLUSIONS: Mortality was most closely associated with right ventricular hemodynamic function and can be characterized by means of an equation using three variables: mean pulmonary artery pressure, mean right atrial pressure, and cardiac index. Such an equation, once validated prospectively, could be used as an adjunct in planning treatment strategies and allocating medical resources.

Adult↗
PubMed2005

Functional valvular incompetence in decompensated heart failure: noninvasive monitoring and response to medical management.

OBJECTIVE: We hypothesized that functional mitral and tricuspid valvular incompetence (MR and TR, respectively) are reversible causes of reduced cardiac output in decompensated heart failure (DF) that accompanies systolic dysfunction in ischemic or nonischemic cardiomyopathy. BACKGROUND: DF, defined as signs and symptoms of heart failure at rest, is rooted in a salt-avid state transduced by neurohormonal activation secondary to impaired renal perfusion. Functional MR and TR are reversible causes of reduced systemic blood flow. Their impact on cardiac output, thoracic fluid content, cardiac chamber dimensions, and valvular apparatus function can be monitored noninvasively, before and after optimized medical management. METHODS: Fourteen male subjects (66 +/- 8 years old) with reduced ejection fraction (24 +/- 5%) secondary to ischemic (71%) or nonischemic (29%) cardiomyopathy, who developed DF with clinical evidence of mitral (MR) and tricuspid (TR) valvular incompetence, were each assessed by bioimpedance and echocardiography before and 1 week after optimized medical management restored compensated failure. RESULTS: Pharmacologic elimination of DF was accompanied by a reduction in body weight (P < 0.01). Hemodynamic improvements included a rise in cardiac index (2.1 to 2.6 L/min/m2; P < 0.01) and a reduction in predicted pulmonary artery systolic pressure (58 to 35 mm Hg; P < 0.001), thoracic fluid content (39 to 32 kOhm; P < 0.001), and systemic vascular resistance (1633 to 1209 dynes/sec/cm5; P < 0.001). Improvements in functional MR and TR included reductions in left and right atrial areas (27 to 24 cm and 26 to 23 cm2, respectively; P < 0.001), color-flow grading of MR and TR severity (P < 0.01), mitral regurgitant volume (105 to 65 mL; P < 0.001), and effective MR orifice size (0.8 to 0.6 cm2; P < 0.01). CONCLUSIONS: In DF, functional MR and TR contribute to reduced cardiac output, increased thoracic fluid content, and systemic vascular resistance, together with enlarged atria and valvular orifice size, which can be improved by medical management. Bioimpedance and echocardiography provide for serial noninvasive assessments of hemodynamic status and valvular function in such cases.

Aged↗
PubMed2001

Monophasic transmitral flow pattern with less increase in heart rate indicates left ventricular dysfunction.

When heart rate (HR) increases, mitral flow can become monophasic. Prolonged isovolumic contraction and relaxation time (ICT and IRT), directly related to left ventricular (LV) function, can potentially influence the HR with monophasic mitral flow. The present study investigated the relation between HR that causes monophasic flow and LV function. During diagnostic catheterization, HR was increased using right atrial pacing by 2 beats/min every 2 min in a stepwise manner until the development of monophasic mitral flow in 17 patients with normal sinus rhythm. ICT, IRT, end-diastolic and end-systolic LV volumes, LV ejection fraction, LV peak + and -dP/dt, peak (+dP/dt)/P, and the relaxation time constant (tau) were measured by Doppler echocardiography or catheterization when monophasic mitral flow developed. The monophasic HR varied from 74 to 106 beats/min. By univariate analysis, ICT (p<0.01, r2=0.73), LV peak +dP/dt (p<0.05, r2=0.37), peak (+dP/dt)/P (p<0.01, r2=0.71), peak -dP/dt (p<0.05, r2=0.25), and tau (p<0.05, r2=0.33) had a significant correlation with monophasic HR. By multivariate analysis, prolonged ICT and reduced LV peak -dP/dt independently contributed to monophasic mitral flow with less increase in HR. Monophasic mitral flow with less increase in HR indicates impaired LV systolic and diastolic function during isovolumic contraction and relaxation.

Adult↗
PubMed1992

Atrial vulnerability and electrophysiology determined in patients with and without paroxysmal atrial fibrillation.

For elucidation of atrial electrophysiology and vulnerability an electrophysiological study was performed in 45 patients with documented paroxysmal atrial fibrillation and a control group (n = 46). Atrial vulnerability was assessed by programmed atrial stimulation with up to two extrastimuli during sinus rhythm and paced cycle lengths of 600 msec, 430 msec and 330 msec. Sustained atrial fibrillation or flutter was induced in 37/45 patients with paroxysmal atrial fibrillation in contrast to 9/46 patients in the control group (P less than 0.001). Left atrial diameter (M-mode echocardiogram), P wave duration, sinus cycle length, sinus node recovery time, and the effective refractory period of the right atrium were not significantly different between the two study groups. Intraatrial conduction time from the high right atrium (HRA) to the basal right atrium (A) and the functional refractory period of the right atrium were significantly longer in patients with paroxysmal atrial fibrillation.

Atrial Fibrillation↗