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PubMed2001

The effects of chronic carvedilol therapy on QT dispersion in patients with congestive heart failure.

BACKGROUND: Carvedilol therapy reduces mortality from sudden cardiac death and progressive pump failure in congestive heart failure (CHF). However, the effect(s) of carvedilol on ventricular repolarization characteristics is unclear. AIM: The aim of the study was to investigate the effects of chronic carvedilol therapy on ventricular repolarization characteristics as assessed by QT dispersion (QTd) in patients with CHF. METHOD: Nineteen patients (age 53+/-12 years; 16 male, three female) with CHF (eight ischemic, 11 non-ischemic dilated cardiomyopathy) were prospectively included in the study. Carvedilol was administered in addition to standard therapy for CHF at a dose of 3.125 mg bid and uptitrated biweekly to the maximum tolerated dose. From standard 12-lead electrocardiograms the maximum and minimum QT intervals (QTmax, QTmin), QTd, corrected QT intervals (QTcmax, QTcmin) and corrected QTd (QTcd) values were calculated at baseline, after the 2nd and the 16th month of carvedilol therapy. RESULTS: A significant reduction was noted in the QTd and QTcd values with carvedilol therapy after the 16th month (QTd: 81+/-22 ms vs. 40+/-4.3 ms P<0.001; QTcd: 91+/-25 ms vs. 51+/-7 ms P<0.001), but not after the 2nd month (P>0.05). The resting heart rate was also significantly reduced after a 16-month course of carvedilol therapy (78+/-13 bpm vs. 66+/-15 bpm, P<0.05). Carvedilol therapy did not alter QTmax and QTcmax intervals (P>0.05), however, QT min and QTcmin significantly increased with carvedilol at the 16th month (P<0.001 and P<0.01, respectively). CONCLUSION: Long-term carvedilol therapy was associated with a reduction in QTd, an effect that might contribute to the favorable effects of carvedilol in reducing sudden cardiac death in CHF.

Adrenergic beta-Antagonists↗

PubMed1978

Angiotensin II blockade in congestive heart failure.

Five of 11 normotensive patients with congestive heart failure responded to an infusion of the specific angiotensin II antagonist, saralasin, by reducing systemic vascular resistance from 2274 +/- 418 to 1690 +/- 351 dynes/sec/cm-5 (mean +/- standard error). This decrease was accompanied by a reduction in left ventricular filling pressure from 19.4 +/- 5.9 to 11.6 +/- 4.0 mm Hg, an increase in cardiac index from 2.2 +/- 0.4 to 2.7 +/- 0.4 l/min/m2 and a decrease in mean arterial pressure from 95 +/- 9.8 to 86 /+- 8.6 mm Hg. In the other 6 patients with congestive heart failure and in 4 controls, saralasin produced either no change or slight increases in systemic vascular resistance. Plasma renin activity did not differentiate responders from non-respnders. Specific inhibition of angiotensin may provide a means for reducing inappropriately high peripheral resistance in some patients with congestive heart failure.

Adult↗

PubMed1990

Comparative hemodynamic effects of intravenous dobutamine and dibutyryl cyclic AMP, a new inotropic agent, in severe congestive heart failure.

In nine patients with chronic congestive heart failure, the acute hemodynamic response to intravenous (i.v.) dibutyryl cyclic AMP (DBcyclicAMP) administration was compared with i.v. dobutamine administration. Both agents led to a significant and similar increase in cardiac index. Dobutamine caused a significant increase in mean arterial pressure but did not produce a significant change in pulmonary capillary wedge, mean pulmonary artery, or mean right atrial pressures. In contrast, DBcyclicAMP caused a significant decrease in mean arterial, mean pulmonary capillary wedge, mean pulmonary artery, and mean right atrial pressures, reflecting vasodilator activity. The fall in systemic vascular resistance was larger after DBcyclicAMP than after dobutamine. DBcyclicAMP achieves an optimal improvement in cardiovascular hemodynamics in concert with substantial vasodilating effect. This pharmacologic action constitutes the mainstay of i.v. therapy for severe congestive heart failure (CHF).

Adult↗

PubMed1989

Opiate receptor inhibition improves the blunted baroreflex function in conscious dogs with right-sided congestive heart failure.

The endogenous opiate system is activated in congestive heart failure. because endogenous opioids are known to depress the baroreflex function, we conducted studies to determine whether the increased endogenous opioids play a role in causing the reduced baroreflex function that occurs in heart failure. Right-sided congestive heart failure was produced in 16 dogs by tricuspid avulsion and progressive pulmonary artery constriction. Seven sham-operated dogs were included for comparison. Baroreflex function was measured in the conscious dogs after pretreatment with either normal saline or an opiate-receptor antagonist by bolus administration of phenylephrine. The slope of the regression line relating systolic blood pressure to cardiac cycle (R-R) interval was taken as an index of baroreflex sensitivity. Plasma beta-endorphin was elevated in the dogs with heart failure (15.3 +/- 2.5 pmol/l) compared with the sham-operated dogs (4.2 +/- 0.4 pmol/l, p less than 0.001). The dogs with heart failure also exhibited a reduced baroreflex sensitivity (3.84 +/- 0.19 msec/mm Hg) after saline pretreatment when compared with the sham-operated dogs (10.86 +/- 1.20 msec/mm Hg, p less than 0.001). Administration of naloxone hydrochloride increased the baroreflex sensitivity of dogs with heart failure to 5.16 +/- 0.26 msec/mm Hg (p less than 0.01) but produced no significant effects in sham-operated dogs (11.36 +/- 1.42 msec/mm Hg). To further study the site of action for the effect of naloxone, we measured baroreflex sensitivity in the dogs with heart failure after pretreatment with naloxonazine, a selective mu-receptor antagonist, with ICI 154,129, a selective delta-receptor antagonist, or with naloxone methobromide, a quaternary analogue of naloxone that does not penetrate the blood-brain barrier.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

The effects of dobutamine, propranolol and nitroglycerin on an experimental canine model of congestive heart failure.

A new experimental model of acute congestive heart failure was established in open-chest dogs, and it was employed to examine the effects of dobutamine, propranolol and nitroglycerin. The model was induced by intracoronary administration of saponin, volume loading and intravenous infusion of methoxamine. Left ventricular end-diastolic pressure (LVEDP) increased from 7.9 +/- 0.6 to 24.2 +/- 1.4 mmHg, and aortic blood flow (AoF) decreased from 0.89 +/- 0.06 to 0.53 +/- 0.04 l/min. Systemic vascular resistance (SVR) increased from 9618 +/- 585 to 16492 +/- 1213 dynes.sec/cm5 and right atrial pressure (RAP) increased from 2.5 +/- 0.2 to 4.2 +/- 0.4 mmHg. Furthermore, Vmax decreased from 71.6 +/- 5.1 to 45.8 +/- 2.9 1/sec, and the time constant of left ventricular pressure decay (T) increased from 40.0 +/- 2.6 to 90.2 +/- 7.9 msec. These hemodynamic changes were stable for up to 80 min. Dobutamine improved cardiac function by increasing Vmax and by decreasing T. Consequently, dobutamine increased AoF and decreased LVEDP, while there was no change in SVR. Nitroglycerin reduced LVEDP, SVR and T; increased AoF; and did not change Vmax. Propranolol produced no improvement in the hemodynamics or cardiac function. These results indicate that the present congestive heart failure model is characterized by global left ventricular dysfunction with lowered cardiac output and increased peripheral vascular tone, and it is beneficial for evaluating the pharmacological properties of drugs for acute congestive heart failure.

Analysis of Variance↗

PubMed1989

Peripheral hemodynamic effects of captopril in patients with congestive heart failure.

In 14 patients with severe congestive heart failure, the effects of captopril on the forearm circulation were evaluated with strain gauge plethysmography. Changes in plasma renin activity, angiotensin II, norepinephrine, epinephrine, bradykinin, prostaglandin E2, and 6-keto-prostaglandin F1 alpha concentrations were also measured. To determine whether the prostaglandins contribute to the peripheral hemodynamic response to captopril, the hemodynamic and hormonal measurements were repeated after pretreatment with indomethacin, an inhibitor of prostaglandin synthesis. Ninety minutes after administering a single dose of captopril (25 mg), mean blood pressure and venous pressure decreased (p less than 0.01 and p less than 0.05, respectively), forearm blood flow and maximum venous volume increased (p less than 0.05 for both), and forearm vascular resistance and forearm venous tone decreased (p less than 0.05 for both). Captopril also improved forearm venous distensibility (p less than 0.05). Pretreatment with oral indomethacin (50 mg) significantly blunted all of these captopril-induced hemodynamic changes. The blockage of the renin-angiotensin system by captopril was unaltered by indomethacin pretreatment. Captopril significantly increased plasma bradykinin, prostaglandin E2, and 6-keto-prostaglandin F1 alpha (p less than 0.05 for each). Indomethacin pretreatment did not affect the captopril-induced increase in bradykinin, but it did completely eliminate the increase in the prostaglandins. Plasma catecholamines did not change with captopril. These data suggest that the vasodilator prostaglandins play a significant role in captopril's peripheral vasodilative effects in congestive heart failure.

6-Ketoprostaglandin F1 alpha↗

PubMed1996

[Current treatments of congestive heart failure].

Mortality in patients with congestive heart failure has been assessed in several large scale multicentric studies, confirming the therapeutic effect of certain treatments and raising questions as to the efficacy of other, sometimes new propositions. Conversion enzyme inhibitors are currently considered to be the first line treatment for heart failure because of their beneficial effect on mortality figures and their capacity to prevent aggravation. These drugs should always be prescribed for patients without contraindications, together with diuretics when signs of congestion develop, and digitalis in case of non-response, then finally nitroglycerin. Debate is still open on the effect of beta-blockers and amiodarone which should be reserved for use by specialists since it has not been definitely proven that they can lengthen survival time. Certain other drugs have given disappointing results compared with early expectations: direct vasodilators, positive inotrops (with the possible exception of vesnarinone), and class Ic antiarrhythmics. Finally several drugs in the development or research stage may prove to be effective in improving heart function, intermediary criteria and, most importantly, survival.

Adrenergic beta-Antagonists↗

PubMed1976

Diuretic and clinical effects of low-dose furosemide in congestive heart failure patients.

A dose of 20 mg furosemide in congestive heart failure patients produces a significant diuretic and natriuretic effect. The peak effect was observed within 60-120 minutes in most patients. Twenty-four congestive heart failure patients were hospitalized for evaluation and management. Two withdrew from the study, and in three there was a prolonged (several months) remission of manifestations of congestive heart failure. The remaining 19 patients were treated with 40 mg furosemide per day for a four-week period. Six required 80 to 120 mg furosemide per day, and 13 were controlled on 40 mg per day. On 20 mg twice per day, one of the 13 patients dropped out voluntarily, two required a higher dose of furosemide, and 10 were controlled on this regimen for a four-week period. When dosage was reduced to 20 mg per day, five of the ten patients were controlled for an additional four weeks or longer, and five required higher doses of furosemide. Results of this study suggest that in congestive heart failure patients, 20 mg furosemide per day has significant diuretic and natriuretic properties. It also demonstrates that a number of patients with cardiac decompensation can be controlled on a relatively low dosage of furosemide and that periodic reevaluation of clinical status and diuretic requirements for maintenance therapy is of critical importance in management of patients with congestive heart failure.

Adult↗

PubMed1988

Congestive heart failure in dialysis patients.

To determine the prevalence of congestive heart failure in dialysis patients and the disorders with which it is associated, 85% of 153 nondiabetic patients who were undergoing maintenance dialysis had echocardiography and gated cardiac scan. Ten percent (n = 15) had congestive heart failure, 53% (n = 8) of whom had dilated cardiomyopathy, and 47% (n = 7) had hypertrophic hyperkinetic cardiomyopathy. Ischemic heart disease was an additional independent risk factor for congestive heart failure. Significantly more of those patients with dilated cardiomyopathy were smokers and none were hypertensive, whereas all those patients with hypertrophic cardiomyopathy were hypertensive. The prevalence of hypertrophic hyperkinetic disease was 11%, of dilated cardiomyopathy 18%, and of symptomatic ischemic heart disease 18%. We concluded that congestive heart failure in dialysis patients is associated not only with dilated cardiomyopathy but also with hypertrophic cardiomyopathy, a disease that requires echocardiography for diagnosis and that has different risk factors and management.

Cardiomyopathy, Dilated↗

PubMed1991

Abnormal baroreflex control of heart rate in decompensated congestive heart failure and reversal after compensation.

Congestive heart failure (CHF) causes impairment of baroreflex control of heart rate (HR). To determine if this derangement is reversible, the cardiac chronotropic control was assessed in 10 patients with class IV chronic CHF of various etiologies before and after compensation achieved by bed rest, salt restriction, diuretics and vasodilators. Mean time between the 2 studies was 15 +/- 3 days. The management was modified 3 days before the second autonomic evaluation, so as to reestablish the same diet and pharmacologic conditions of the previous study. Compensation led to significant reduction in symptom-based class, body weight, and pulmonary and systemic congestion. Mean +/- standard error of the mean HR responses (beats/min) before and after compensation were, respectively: (1) to atropine (0.04 mg/kg): 10 +/- 2 and 27 +/- 2 (p less than 0.01); (2) to handgrip (30% maximum capacity, 1 minute): 9 +/- 2 and 19 +/- 3 (p less than 0.005); (3) to headup tilt (5 minutes): 4 +/- 3 and 20 +/- 4 (p less than 0.005). Mean +/- standard error of the mean baroreflex sensitivity (ms/mm Hg) of RR responses to phenylephrine and amyl nitrate-induced changes in systolic pressure was, respectively, in each condition: phenylephrine, 0.9 +/- 0.2 and 8 +/- 2.3 (p less than 0.05); amyl nitrate, 0.3 +/- 0.2 and 4.1 +/- 1.1 (p less than 0.05). A significant correlation between improvement in HR responses to atropine and tilt and changes in body weight was obtained. These findings show a reversible component of impaired baroreflex control of HR in severe CHF, possibly due to its congestive effects.

Adaptation, Physiological↗

PubMed2002

Alcohol consumption and risk for congestive heart failure in the Framingham Heart Study.

BACKGROUND: Although excessive alcohol consumption can promote cardiomyopathy, little is known about the association between alcohol consumption and risk for congestive heart failure in the community. OBJECTIVE: To determine the relation between alcohol consumption and risk for congestive heart failure in the community. DESIGN: Community-based, prospective observational study. SETTING: Framingham, Massachusetts. PARTICIPANTS: Participants in the Framingham Heart Study who were free of congestive heart failure and coronary heart disease. MEASUREMENTS: Self-reported alcohol consumption; sex-specific rates of congestive heart failure per 1000 person-years of follow-up by level of alcohol consumption. RESULTS: In men, 99 cases of congestive heart failure occurred during 26 035 person-years of follow-up. In women, 120 cases of congestive heart failure occurred during 35 563 person-years of follow-up. After adjustment for multiple confounders, risk for congestive heart failure was lower among men at all levels of alcohol consumption compared with men who consumed less than 1 drink/wk. The hazard ratio for congestive heart failure was lowest among men who consumed 8 to 14 drinks/wk (0.41 [95% CI, 0.21 to 0.81]) compared with those who consumed less than 1 drink/wk. In women, the age-adjusted hazard ratio for congestive heart failure was lowest among those who consumed 3 to 7 drinks/wk (0.49 [CI, 0.25 to 0.96]) compared with those who consumed less than 1 drink/wk. However, after adjustment for multiple predictors of congestive heart failure, this association was no longer statistically significant. CONCLUSIONS: In the community, alcohol consumption is not associated with increased risk for congestive heart failure, even among heavy drinkers (> or = 15 drinks/wk in men and > or = 8 drinks/wk in women). To the contrary, when consumed in moderation, alcohol appears to protect against congestive heart failure.

Adult↗

PubMed1998

Carvedilol: preclinical profile and mechanisms of action in preventing the progression of congestive heart failure.

Many pathophysiological processes are activated in patients with congestive heart failure, and several of these have been implicated in the progression of the disease. The most important processes to be activated in heart failure are the neurohormonal systems, which include the reninangiotensin system, the sympathetic nervous system and the endothelin system. In addition to the neurohormonal systems, the formation of reactive oxygen free radicals is increased in congestive heart failure. It has been proposed that the activation of neurohormonal pathways and the formation of oxygen free radicals ultimately lead to the activation of a family of transcription factors that are involved in cardiac and vascular remodelling which are hallmarks of congestive heart failure. In addition, the formation of oxygen free radicals has been implicated in the process of apoptosis, or programmed cell death, which may contribute to the continued loss of myocardial cells resulting in progressive decreases in left ventricular function, while at the same time contributing to the cardiac remodelling process which subsequently creates a pro-arrhythmic environment in the myocardium. Carvedilol is a novel multiple-action neurohormonal antagonist that has been shown to be effective in the management of congestive heart failure. Carvedilol also possesses a number of additional activities which may inhibit many of the chronic pathophysiological processes that are involved in the progression of congestive heart failure.

Adrenergic alpha-Antagonists↗

PubMedDate not supplied

Congestive heart failure: new paradigms and therapeutic targets.

Congestive heart failure is a major clinical and public health challenge. With increased aging, and advanced care of almost all other cardiac diseases, myocardial failure has become the single most common reason for hospitalization for patients older than 65. Conventional wisdom addressed heart failure as a hemodynamic perturbation consisting of congestion and limited cardiac output. Efforts intuitively focused on augmenting systolic function and clearing excessive pulmonary and systemic edema. Despite symptomatic improvement, mortality and functional deterioration continued unabated. Afterload reducing therapy emerged as an effective modality of improving cardiac function. Selective targeting of renin-angiotensin-aldosterone system (RAAS) was shown to be superior to alternative nonhormone-based approaches. These clinical observations gave impetus to the neurohumoral paradigm of heart failure. Whereas attention to the congestive aspects of heart failure remains an essential component of therapy, it is by no means sufficient to neutralize the complex and interactive pathogenic mechanisms which underlie this syndrome. Particularly relevant, is the asymptomatic stage of ventricular dysfunction which portend significant future structural and functional deterioration. Mounting evidence confirm the benefit of ACEI and ARB in attenuating ventricular remodeling and improving survival. This paper aims at reviewing the evidence which has led to the strongly held paradigm of neurohormonal basis of heart failure. Appropriate and evidence based therapeutic strategies are presented.

Adrenergic beta-Antagonists↗

PubMed1997

Current and newer approaches in the drug treatment of congestive heart failure.

Most patients with chronic congestive heart failure (CHF) are subjected to symptomatic treatment, predominantly with drugs. Over the years, it has become clear that treatment with unloading drugs is probably more beneficial than treatment with inotropic agents. In addition, it has been widely recognized that the neuroendocrine compensatory changes associated with CHF afford and important target for drug treatment. This may also hold for some of the changes in receptor density, such as the downregulation of cardiac beta-adrenoceptors. The present and clearly changing insights into the backgrounds of drugs for the treatment of CHF are critically discussed. Apart from the changing views and appreciation of the currently used drugs (diuretics, ACE inhibitors, digoxin, beta-adrenoceptor agonists), the following new approaches are discussed: beta-blockers, angiotensin II receptor antagonists, ibopamine, calcium antagonists, inhibitors of ANP degradation, vasopression antagonist, vesnarinone, and calcium sensitizers.

Adrenergic beta-Agonists↗

PubMed1981

Beneficial hemodynamic response to chronic prazosin therapy in congestive heart failure.

Thirteen patients with advanced congestive heart failure (CHF) were treated with prazosin. Following the first dose, cardiac output (CO) (mean +/- SD) rose from 3.2 +/- 1.2 to 4.3 +/- 1.1 L/min, pulmonary artery diastolic pressure (PAD) decreased from 23 +/- 12 to 18 +/- 11 mm Hg, mean arterial pressure (MAP) decreased from 85 +/- 10 to 76 +/- 10 mm Hg, and heart rate did not change (92 +/- 15 vs 92 +/- 14 bpm). At the end of a 48 to 72 hour titration to an optimal regimen, significant effects on CO (3.2 +/- 1.1 vs 4.5 +/- 1.3 L/min), PAD (24 +/- 12 vs 18 +/- 8 mm Hg), and MAP (84 +/- 10 vs 76 +/- 10 mm Hg) were still seen. The patients were restudied after 3 months of treatment. In contrast to reports of rapid development of tolerance to prazosin, we found continued beneficial effects on CO (3.0 +/- 1.3 vs 3.8 +/- 1.0 L/min) and PAD (23 +/- 12 vs 18 +/- 10 mm Hg), without significant change in MAP (81 +/- 11 vs 78 +/- 8 mm Hg). We found wide variability in the CO rise in response to prazosin, which was not accounted for by differences in plasma prazosin concentration. Systemic vascular resistance in the untreated state did correlate with the percentage change in CO. In addition, excessive lowering of the PAD appeared to blunt the CO response in some cases.

Blood Pressure↗

PubMed1981

Pirbuterol: a new oral sympathomimetic amine for the treatment of congestive heart failure.

Fourteen patients with refractory congestive heart failure (CHF) were given a single oral dose ranging from 5 to 30 mg of the new sympathomimetic drug pirbuterol. Hemodynamic measurements and plasma pirbuterol levels were obtained at control and then serially for 6 hours following drug administration. The optimal pirbuterol dose range was determined to be 20 to 30 mg. Ten patients received 20 to 30 mg pirbuterol. In this group cardiac index was significantly increased (1.9 to 2.6 L/min/m2, p less than 0.001). Pulmonary artery wedge pressures fell significantly (24 to 20 mm Hg, p less than 0.02). Decreases were also noted in mean pulmonary artery pressure (36 to 31 mm Hg, p less than 0.02), aortic diastolic pressure (71 to 65 mm Hg, p less than 0.05), systemic vascular resistance (1782 to 1201 dynes. sec. cm-5, p less than 0.001), and pulmonary vascular resistance (265 to 175 dynes.sec.cm-5, less than 0.001). Systolic and mean aortic pressure and heart rate showed no significant change from control. Hemodynamic effects persisted for 5 hours. Pirbuterol was clinically well tolerated. The mechanism of action is unclear at this time, but both inotropic and vasodilator effects are possible. Pirbuterol orally has a marked and prolonged salutary hemodynamic effect and offers promise in CHF treatment.

Administration, Oral↗

PubMed1982

Relationship of exercise capacity to resting left ventricular performance and basal plasma norepinephrine levels in patients with congestive heart failure.

Seventeen patients with chronic congestive heart failure (CHF) were studied to assess the relationship of resting left ventricular function, as measured by noninvasive and invasive methods, to maximal exercise capacity, as measured by peak total body oxygen consumption (VO2). Supine basal plasma norepinephrine (NE) was also measured to evaluate its relationship to the severity of heart failure and to determine whether it may be a better predictor of exercise capacity in patients with CHF than the more commonly employed noninvasive and invasive tests of left ventricular function. Fourteen of the 17 patients underwent upright bicycle exercise (average peak VO2 10.60 +/- 1.40 ml/kg/min, +/- SEM) to their symptomatic maximum. There was no significant correlation between peak VO2 and the noninvasive measurements of left ventricular performance obtained at rest, including cardiothoracic ratio, left ventricular internal dimension by M-mode echo, percent shortening of the minor axis by M-mode echo, and radionuclide ejection fraction. Hemodynamic measurements were performed in 16 patients. The hemodynamic measurements at rest also failed to correlate with exercise capacity. The supine basal plasma NE, which was elevated in these 17 patients (612 +/- 100 pg/ml), had an inverse relationship with stroke work index (r - -0.70, p less than 0.01) and stroke index (r = -0.83, p less than 0.001) and a positive correlation with right atrial pressure (r = 0.81, p less than 0.001). Although both noninvasive and invasive measurements at rest failed to correlate significantly with peak VO2 during exercise, the plasma NE had a significant inverse correlation with peak exercise VO2 (r = -0.50, p less than 0.05). The basal supine plasma NE is therefore elevated in patients with CHF, is a marker for the severity of CHF as measured by hemodynamics performed at rest, and is a better predictor of exercise capacity than standard noninvasive and invasive tests performed at rest.

Adult↗

PubMed1995

Doppler echocardiographic pulmonary venous flow-velocity pattern for assessment of the hemodynamic profile in acute congestive heart failure.

The hemodynamic profile of congestive heart failure (CHF) is best described in terms of its two primary sets of hemodynamic parameters, that is, left atrial pressure and cardiac output, each of which has a specific and independently variable hemodynamic cause. To assess whether analysis of the mitral and/or pulmonary venous flow-velocity patterns provides valuable information in the noninvasive assessment of the hemodynamic profile of CHF, these patterns were obtained by using the transthoracic approach in 18 patients with acute CHF with simultaneous measurements of catheter-derived mean pulmonary capillary wedge pressure and thermodilution cardiac index. Measurements were repeated on two occasions in each case: at the acute stage of CHF and 1 to 5 days after treatment. Peak diastolic pulmonary venous forward flow velocity was higher, the ratio of pulmonary venous systolic to diastolic peak forward flow velocity was lower, and the ratio of mitral early diastolic to late diastolic flow velocity was greater in patients with higher mean pulmonary capillary wedge pressure (r = 0.80, n = 36, p < 0.01; r = -0.69, n = 36, p < 0.01; r = 0.71, n = 36, p < 0.01). Peak systolic pulmonary venous forward flow velocity and time-velocity integral of the systolic pulmonary venous flow wave were greater in patients with larger cardiac index (r = 0.80, n = 36, p < 0.01; r = 0.62, n = 36, p < 0.01). In conclusion, two primary sets of hemodynamic parameters, that is, left atrial pressure and cardiac output, can be estimated with Doppler pulmonary venous flow parameters in patients with acute CHF.

Acute Disease↗