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PubMedDate not supplied

Pulmonary venous flow in cardiac tamponade: influence of left ventricular dysfunction and the relation to pulsus paradoxus.

The pattern of left atrial filling was studied in nine closed-chest dogs during cardiac tamponade before and after production of microembolic left ventricular dysfunction produced by intracoronary injection of 54 +/- 4 microns (SD) microspheres. With cardiac tamponade, a significant increase in the ratio of systolic/diastolic pulmonary venous flow velocity integral both before (1.65 +/- 0.24 versus 2.77 +/- 0.43 [SE], p less than 0.05) and after production of left ventricular dysfunction (0.57 +/- 0.12 versus 1.77 +/- 0.44, p less than 0.05) was seen. Compared with baseline, cardiac tamponade caused a significant inspiratory decrease in systolic pulmonary venous velocity both before (7.3 +/- 2.0 versus 1.2 +/- 1.4 cm/sec) and after left ventricular dysfunction (3.4 +/- 0.4 versus 1.0 +/- 0.9 cm/sec, both p less than 0.05). The magnitude of respiratory variation (expiration-inspiration) of the pulmonary venous flow velocity integral with tamponade was significantly greater before than after left ventricular dysfunction (1.6 +/- 0.2 cm versus 0.8 +/- 0.2 cm, p less than 0.05). A significant correlation was found between the inspiratory fall in aortic systolic pressure and the flow velocity integral of pulmonary venous flow before left ventricular dysfunction (r = 0.58, p less than 0.05). After coronary embolization, neither pulsus paradoxus nor significant respiratory variation (expiration-inspiration) of the pulmonary venous flow integral was observed with cardiac tamponade. In this model of cardiac tamponade and left ventricular dysfunction, left atrial filling occurs predominantly during ventricular systole. These changes may be helpful in recognizing hemodynamically significant pericardial effusion and have implications for the pathophysiology of cardiac tamponade.

Animals↗

PubMed1990

Silent left ventricular dysfunction during routine activity after thrombolytic therapy for acute myocardial infarction.

To investigate prospectively the occurrence and significance of postinfarction transient left ventricular dysfunction, 33 ambulatory patients who underwent thrombolytic therapy after myocardial infarction were monitored continuously for 187 +/- 56 min during normal activity with a radionuclide left ventricular function detector at the time of hospital discharge. Twelve patients demonstrated 19 episodes of transient left ventricular dysfunction (greater than 0.05 decrease in ejection fraction, lasting greater than or equal to 1 min), with no change in heart rate. Only two episodes in one patient were associated with chest pain and electrocardiographic changes. The baseline ejection fraction was 0.52 +/- 0.12 in patients with transient left ventricular dysfunction and 0.51 +/- 0.13 in patients without dysfunction (p = NS). At follow-up study (19.2 +/- 5.4 months), cardiac events (unstable angina, myocardial infarction or death) occurred in 8 of 12 patients with but in only 3 of 21 patients without transient left ventricular dysfunction (p less than 0.01). During submaximal supine bicycle exercise, only two patients demonstrated a decrease in ejection fraction greater than or equal to 0.05 at peak exercise; neither had a subsequent cardiac event. These data suggest that transient episodes of silent left ventricular dysfunction at hospital discharge in patients treated with thrombolysis after myocardial infarction are common and associated with a poor outcome. Continuous left ventricular function monitoring during normal activity may provide prognostic information not available from submaximal exercise test results.

Acute Disease↗

PubMed2002

Long-term outcome after coronary artery bypass grafting in patients with severe left ventricular dysfunction.

BACKGROUND: The aim of this study was to define the potential for long-term survival with severe left ventricular dysfunction after coronary bypass and to quantify any improvement in overall functional status. METHODS: Left ventricular dysfunction was confirmed preoperatively and the long-term survival and functional outcome after bypass was determined by follow-up studies obtained during the span of a decade. RESULTS: From 1/1990 to 12/1999, 86 patients with severe left ventricular dysfunction (mean ejection fraction, 0.18 +/- 0.03; range, 0.10 to 0.20) underwent coronary artery bypass grafting. There were 10 perioperative deaths (11% mortality). The mean survival was 55 months (standard deviation +/- 34 months; range, 2 to 141 months) with an actual 5-year survival rate of 59% (actuarial 5-year 65%, 10-year 33%). Echocardiography obtained between 1 and 6 months, 6 months and 1 year, 1 and 2 years, 2 and 4 years, 4 and 6 years, and 6 and 11 years showed the ejection fraction improved to 0.29 +/- 0.08 (p < 0.001), 0.31 +/- 0.14 (p < 0.002), 0.35 +/- 0.08 (p < 0.001), 0.27 +/- 0.10 (p = 0.002), 0.36 +/- 0.14 (p = 0.004), and 0.30 +/- 0.11 (p = 0.004), respectively. At 1 to 6 months, 6 months to 1 year, and 1 to 2 years, the diastolic left ventricular dimension was unchanged, but the systolic left ventricular dimension decreased significantly from 5.02 +/- 0.77 cm to 4.26 +/- 0.91 cm (p = 0.046), 3.98 +/- 1.43 cm (p = 0.08), and 4.10 +/- 1.14 cm (p = 0.07). The preoperative New York Heart Association classification for all patients improved from 2.8 +/- 0.8 to 1.6 +/- 0.7 (p < 0.001) after a mean of 53 months (standard deviation +/- 34 months). CONCLUSIONS: Patients with severe left ventricular dysfunction can derive long-term benefit from coronary bypass through improved left ventricular contractility as documented by a significantly decreased systolic left ventricular dimension and increased ejection fraction. Successful bypass is associated with a 59% actual 5-year survival rate and significantly improved New York Heart Association functional class.

Actuarial Analysis↗

PubMed2003

Significant effects of atrioventricular node ablation and pacemaker implantation on left ventricular function and long-term survival in patients with atrial fibrillation and left ventricular dysfunction.

Control of ventricular rate by atrioventricular node ablation and pacemaker implantation in patients with drug-refractory atrial fibrillation (AF) is associated with improved left ventricular (LV) function. The objective of this study was to determine the effect of atrioventricular node ablation on long-term survival in patients with AF and LV dysfunction. Survival was determined by the Kaplan-Meier method for 56 study patients with LV ejection fraction (EF) < or =40% who underwent atrioventricular node ablation and pacemaker implantation and 56 age- and gender-matched control patients with AF and LVEF >40%, and age- and gender-matched control subjects from Minnesota. Groups were compared using the log-rank test. In study patients (age 69 +/- 10 years; 45 men), LVEF was 26% +/- 8% and 34% +/- 13% (p <0.001) before and after ablation, respectively. During follow-up (40 +/- 23 months), 23 patients died. Observed survival was worse than that of normal subjects (p <0.001) and control patients (p = 0.005). After ablation, LVEF nearly normalized (> or =45%) in 16 study patients (29%), in whom observed survival was comparable to that of normal subjects (p = 0.37). Coronary artery disease, hyperlipidemia, chronic renal failure, previous myocardial infarction, and coronary artery operation were independent predictors for mortality. Near normalization of LVEF occurred in 29% of study patients, suggesting that AF-induced EF reduction is reversible in many patients. Normal survival in patients with reversible LV dysfunction highlights potential survival benefits of rate control. Poor survival in patients with persistent LV dysfunction confirms the importance of optimal medical therapy.

Aged↗

PubMed1995

Long-term outcome of left ventricular dysfunction after surgery for severe aortic stenosis.

Thirteen patients with severe aortic stenosis and left ventricular dysfunction (ejection fraction < 0.50, Group A) received echocardiographic evaluation before, and early and late after isolated aortic valve replacement. The results were compared with those of 11 aortic stenosis patients without left ventricular dysfunction (Group B). Using two-dimensional echocardiography, left ventricular diastolic internal diameter (LVIDd), left ventricular systolic internal diameter (LVIDs), left ventricular wall thickness (interventricular septum + posterior wall: LVWT), left ventricular fractional shortening (FS), left ventricular mass index (LVMI) and left ventricular end-systolic wall stress (ESWS) were assessed before (Pre), at one month (Early) and 4-7.6 (mean 5.5 +/- 1.0) years (Late) after operation. In the early postoperative period in Group A, significant decrease was observed in LVIDd (5.4 +/- 0.8 to 4.5 +/- 1.0 cm, p = 0.010), LVWT (3.3 +/- 0.7 to 2.9 +/- 0.7 cm, p = 0.027) and LVMI (336 +/- 149 to 222 +/- 112 g/M2, p = 0.013). From the early to late postoperative period FS showed significant improvement in both groups (0.23 +/- 0.12 to 0.32 +/- 0.12 in Group A, p = 0.025 and 0.27 +/- 0.07 to 0.36 +/- 0.07, p = 0.014). However, changes of other parameters were not significant and LVMI in Group A remained twice as high as the normal value. It is concluded from the above results, that LV contraction in aortic stenosis patients with preoperative left ventricular dysfunction improved during the late postoperative period. Although LVMI in the early postoperative period significantly decreased as compared with the preoperative value, it showed no further improvement and remained at an abnormally high level. Therefore, early surgical treatment of severe aortic stenosis before appearance of LV dysfunction should be recommended for postoperative recovery from LV hypertrophy.

Aged↗

PubMed2003

Immediate and late results of coronary angioplasty in patients with severe left ventricular dysfunction.

BACKGROUND: Severe coronary artery disease in patients with a markedly depressed left ventricular function is associated with a poor prognosis. Even though coronary angioplasty (PTCA) has been offered as an alternative to bypass surgery, the role of PTCA in the treatment of patients with severe left ventricular dysfunction has not been well defined. The aim of the present study was to evaluate the immediate and long-term results in patients with severe left ventricular dysfunction < or = 35% who underwent PTCA. METHODS: One hundred and twenty-five patients with a left ventricular ejection fraction < or = 35% who underwent PTCA were analyzed. RESULTS: The mean left ventricular ejection fraction was 29.7%. Eighty-seven patients (69.6%) had multivessel disease and 41 (32.8%) had previous coronary artery bypass graft. Intra-aortic balloon pumping was used in 12% of cases. Angiographic success was achieved in 96% of patients. Complete revascularization was achieved in 56 patients (44.8%). Major complications occurred in 4% of the population and 2 patients died (1.6%). During the long-term follow-up re-PTCA due to angiographic restenosis was performed in 41 patients (34%); 12 patients (10.4%) died. The only parameter which significantly correlated with death was the presence of an occluded left anterior descending coronary artery not recanalized neither with PTCA nor with coronary artery bypass graft. CONCLUSIONS: These data suggest that PTCA may be an effective treatment for coronary artery disease in patients with left ventricular dysfunction and is associated with high procedural success rate and low complications; however, the long-term follow-up seems not to be influenced by the PTCA procedure.

Adult↗

PubMed2004

N-terminal probrain natriuretic peptide (NT-proBNP) in the emergency diagnosis and in-hospital monitoring of patients with dyspnoea and ventricular dysfunction.

OBJECTIVE: To evaluate the utility of NT-proBNP in the emergency diagnosis and in-hospital monitoring of patients with acute dyspnoea and ventricular dysfunction. BACKGROUND: Misdiagnosis of heart failure (HF) is common in the urgent care setting using clinical diagnostic tests. Reports show that BNP is useful to diagnose HF in patients with acute dyspnoea. METHODS: Prospective study of 100 patients attending the Emergency Department (ED) for acute dyspnoea. Final diagnosis was determined on the basis of ED data sheets, echocardiography and pulmonary function tests. NT-proBNP levels were obtained on admission, at 24 h and at day 7. RESULTS: Patients with ventricular dysfunction were sub-classified into decompensated HF and masked HF, defined as HF with concomitant signs of pulmonary disease. Decompensated and masked HF patients had significantly higher NT-proBNP values than patients with non-cardiac dyspnoea (normal ventricular function) (920+/-140 and 978+/-363 vs. 50+/-15 pmol/L; P<0.001 and P<0.01, respectively). The mean area under the ROC curve for NT-proBNP was 0.957 (95% CI, 0.918 to 0.996, P<0.001). In multiple logistic-regression analysis NT-proBNP>115 pmol/l was the strongest independent predictor of ventricular dysfunction (odds ratio 45.4; 95% CI: 4.5-452.3). At day 7, a significant and similar reduction in NT-proBNP was observed in the two groups of patients with ventricular dysfunction (P<0.001 vs. admission values), but complete clinical resolution was less frequent in masked HF patients (P<0.05 vs. decompensated HF). CONCLUSIONS: NT-proBNP is a new candidate marker for the detection and exclusion of ventricular dysfunction in patients attending the ED for acute dyspnoea. NT-proBNP may also serve to monitor outcome during hospitalization.

Adult↗

PubMed1983

Blood pressure and left ventricular dysfunction in the spontaneously hypertensive rat.

The important role of the heart in the manifestation of systemic hypertension often becomes apparent with the development of left ventricular dysfunction. After a prolonged course of stable compensated left ventricular hypertrophy, spontaneously hypertensive rats (SHR) developed left ventricular dysfunction. A phase of overt left ventricular dysfunction and dilatation was present at an advanced age (24 months) in female SHR, a phase during which systemic hypertension was no longer manifest despite the maintenance of an increased vascular resistance. Similarly, when left ventricular dysfunction was induced after the experimental production of a myocardial infarction, the systemic arterial pressure levels of young SHR fell. This reduction in blood pressure was directly related to the extent of the histologic damage to the left ventricle. These studies underscore the important permissive role of the heart in the expression and maintenance of systemic hypertension.

Aging↗

PubMed1985

Use of impedance cardiography in evaluating the exercise response of patients with left ventricular dysfunction.

Invasive studies in patients with left ventricular dysfunction show that data at rest (e.g. ejection fraction-EF) are poor predictors of the changes in cardiac output (CO) which occur with exercise. This investigation was undertaken to determine whether impedance cardiography could be used in such patients to assess CO response to exercise. The method was compared with the direct Fick method. Over a range of COs between 4 and 18 min-1 there was no systematic error. Reproducibility for CO over one week was highly significant (r = 0.94; P less than 0.001). Impedance cardiography was incorporated into routine exercise testing on a bicycle ergometer for a group of 15 patients (mean age 53.2 +/- 3.0 yrs, SEM) who had sustained a major myocardial infarct 6 to 12 months previously, (EF 38.1 +/- 3.5%, SEM). CO was measured at the end of each 3-min stage. In eight patients (EF 40.0 +/- 3.4%, SEM) CO response was abnormal with either a decrease or a failure to increase with increasing workloads. Conventional end-points i.e. angina, attainment of 85% of predicted maximum heart rate, abnormal blood pressure response or excessive dyspnoea did not indicate consistently a need to terminate the test. It is suggested that impedance cardiography is a useful non-invasive method of evaluating patients with left ventricular dysfunction.

Adult↗

PubMed1996

Prognostic value of dobutamine echocardiography in patients with left ventricular dysfunction.

OBJECTIVES: This study sought to establish the prognostic implications of ischemic and viable myocardium identified by dobutamine echocardiography in patients with left ventricular dysfunction. BACKGROUND: Recent studies have suggested that in patients with viable myocardium identified by positron emission tomography, medical treatment is associated with recurrent cardiac events. Dobutamine echocardiography has been used to identify viable myocardium in patients with left ventricular dysfunction, but the prognostic significance of this test is undefined. METHODS: One hundred thirty-six consecutive patients (mean [+/- SD] age 67 +/- 7.9 years; 104 men) with moderate or severe left ventricular dysfunction (left ventricular ejection fraction 30 +/- 5%) undergoing dobutamine echocardiography were included in the study. Dobutamine was administered using a standard incremental protocol (5 to 40 micrograms/kg body weight per min intravenously in 3-min stages) with additional atropine (1 mg intravenously) as required. Standard body weight echocardiographic views were digitized on-line and compared using a side-by-side display. Viable myocardium was identified by enhancement of regional function at low dose (< 10 micrograms); scar was diagnosed by akinesia at rest or dyskinesia without change and ischemia as new or worsening dysfunction. One hundred thirty patients (95%) were followed up for 16 +/- 8 months after the original study for major cardiac events (cardiac death, myocardial infarction or severe unstable angina requiring late myocardial revascularization). RESULTS: No significant complications occurred during dobutamine echocardiography. Viable myocardium was detected in 26 patients (19%), ischemia in 23 (17%), both viability and ischemia in 13 (10%) and scar in 74 (54%). Of 108 patients treated medically, 46 had viable or ischemic myocardium, and 62 had scar only. There were no significant differences in age or other clinical characteristics, stress response, left ventricular dimensions and ejection fraction between the two groups. Cardiac events occurred in 26 medically treated patients (24%): 18 died of cardiac-related causes; 4 had a nonfatal myocardial infarction; and 4 had late revascularization because of unstable angina. The event rate was greater in patients with viable or ischemic myocardium than those with scar (43% vs. 8%, p = 0.01 by log-rank test). In a Cox regression model, the presence of viable or ischemic myocardium was found to predict subsequent events (relative risk 3.51, p = 0.02) independently of ejection fraction and age. CONCLUSIONS: Viable or ischemic myocardium detected at dobutamine echocardiography in patients with left ventricular dysfunction is associated with an adverse prognosis, independent of age and ejection fraction.

Aged↗

PubMed2003

Third heart sound and elevated jugular venous pressure as markers of the subsequent development of heart failure in patients with asymptomatic left ventricular dysfunction.

PURPOSE: To determine the independent prognostic value of a third heart sound (S(3)) and elevated jugular venous pressure in patients with asymptomatic left ventricular dysfunction. METHODS: We performed a post hoc analysis of 4102 participants from the Studies of Left Ventricular Dysfunction (SOLVD) prevention trial. In that trial, participants with asymptomatic or minimally symptomatic left ventricular dysfunction (New York Association class I or II, left ventricular ejection fraction < or =0.35, no treatment for heart failure) were allocated randomly to enalapril or placebo and followed for a mean (+/- SD) of 34 +/- 14 months. The presence of an S(3) and elevated jugular venous pressure was ascertained by physical examination at study enrollment. We used multivariate proportional hazards models to determine whether these physical examination findings were associated with the development of heart failure, a prespecified endpoint of the SOLVD prevention trial. RESULTS: At baseline, 209 subjects (5.1%) had an S(3) and 70 (1.7%) had elevated jugular venous pressure. Heart failure developed in 1044 subjects (25.5%). After adjusting for other markers of disease severity, an S(3) was associated with an increased risk of heart failure (relative risk [RR] = 1.38; 95% confidence interval [CI]: 1.09 to 1.73; P = 0.007) and the composite endpoint of death or development of heart failure (RR = 1.34; 95% CI: 1.09 to 1.64; P = 0.005). Elevated jugular venous pressure was also associated with these outcomes in multivariate models. CONCLUSION: The physical examination provides prognostic information among patients with asymptomatic or minimally symptomatic left ventricular dysfunction.

Analysis of Variance↗

PubMed1997

Right ventricular dysfunction persists following brief right ventricular pressure overload.

OBJECTIVE: Acute pulmonary hypertension may cause right ventricular (RV) contractile failure. While it has been assumed that restoration of normal loading conditions after acute pulmonary hypertension is sufficient for complete recovery of RV function, this has not been rigorously examined. The purpose of this study was to test the hypothesis that acute RV pressure overload produces RV contractile dysfunction that persists following restoration of control loading conditions. METHODS: We subjected 18 autonomically-blocked, chloralose-anesthetized, open-chest pigs to 1 h of pulmonary artery constriction to increase RV systolic pressure from 35 +/- 1 to 55 +/- 1 mmHg, followed by 2 h of measurements after pulmonary artery constriction release. We determined regional RV free wall function from pressure-segment length loops and preload recruitable stroke work relations, and global RV function from stroke work vs. end-diastolic pressure relations. RESULTS: As expected, RV free wall systolic shortening diminished during pulmonary artery constriction, but the endo/epi blood flow ratio, lactate uptake, and coronary venous pH were not significantly changed. Following release of pulmonary artery constriction, RV systolic and diastolic pressure returned to control values. Nonetheless, contractile dysfunction persisted, with depressed RV free wall systolic shortening (70 +/- 22% of control), RV regional external work (59 +/- 11% of control at control end-diastolic length), and global RV stroke work (56 +/- 14% of control at control end-diastolic pressure). Depressed regional work was due to a parallel, rightward shift of the preload recruitable stroke work relation. Five pigs identically instrumented but not subjected to pulmonary artery constriction showed no significant over 3 h. CONCLUSIONS: Acute pulmonary hypertension causes RV contractile dysfunction that persists at least 2 h after restoration of control loading conditions. Contractile dysfunction is not attributable to RV ischemia during pressure overload.

Acute Disease↗

PubMed1984

Natural history of severe left ventricular dysfunction after myocardial infarction.

The prevalence and prognosis of severe left ventricular dysfunction after infarction was prospectively analyzed in a series of 259 male patients aged 60 years or less surviving an acute myocardial infarction. All patients underwent coronary angiography 30 days after the acute event and were followed up for a mean period of 34 months (range, 15 to 55 months). Forty-five patients (17 percent) were found to have severe left ventricular dysfunction (ejection fraction less than or equal to 30 percent). Comparison of patients with and without severe impairment of left ventricular function showed the former to have a lower cardiac index (p less than 0.001), higher left ventricular end-diastolic volume index (p less than 0.001), and a higher prevalence of three-vessel disease (p less than 0.025) and of total or subtotal occlusion of at least one coronary artery (p less than 0.025). While the occurrence of congestive heart failure was higher in patients with severe left ventricular dysfunction (p less than 0.001), the probability of developing angina was similar in both groups. Cox's regression analysis showed ejection fraction to be the only independent predictor of survival in patients with severe impairment of left ventricular function. An ejection fraction of 20 percent or less identified a subset of patients with the highest mortality (62 percent at four years), significantly different from that of patients whose ejection fraction was between 21 and 30 percent (28 percent) (p less than 0.001).

Adult↗

PubMed1999

[Severe ventricular dysfunction. When should is surgery not indicated?].

The decision to operate in the presence of severe ventricular dysfunction is one of the most difficult medical judgements because ventricular dysfunction is, as we know, the leading risk factor for morbidity and mortality in cardiac surgery. However, despite the greater surgical risk in some pathologies, the patients with severe cardiac dysfunction are those who will most likely benefit from surgery when we compare medical and surgical survival curves. Although ejection fraction is the parameter usually used to quantify ventricular systolic function and to stratify patients according to risk, we should not ignore the limitations of this parameter in the evaluation of myocardial function. Therefore, besides ejection fraction, other criteria should be considered in the process of patient selection for surgery. Taking these facts into consideration, the author seeks to establish criteria for different cardiac pathologies for the surgical treatment of patients with severe left ventricular dysfunction.

Coronary Disease↗

PubMed1994

Neurohormones in patients with ischemic left ventricular dysfunction.

Measurements of plasma neurohormones in patients with left ventricular dysfunction are generally performed for research purpose rather than for diagnostic purpose or to guide therapy. These studies have shown that in patients with left ventricular dysfunction, several neurohormonal systems were activated, even in the absence of symptoms of congestive heart failure. This suggested that the cardiovascular system was not in a steady state and pointed out potential culprits for the progression of the disease. It has also been shown that the levels of several of these markers, particularly plasma norepinephrine, had an important prognostic value. Another value of neurohormonal studies obviously is the design of new therapeutic approaches aimed at improving symptoms and prognosis. In this respect, important therapeutic successes have been obtained with agents that interfere with the actions of some of these neurohormonal systems, such as with the use of the angiotensin-converting enzyme (ACE) inhibitors, particularly captopril and enalapril, and to a lesser extent, with beta-blockers. It can therefore be expected that, in the future, most patients with severe ischemic dysfunction will be treated with an ACE inhibitor. Nonetheless, neurohormonal control is not complete with these drugs; powerful vasoconstrictor forces, such as endothelin-1, remain activated, and an escape of angiotensin II from the control of ACE inhibition may exist. Thus, morbidity (e.g., progression towards congestive heart failure and angina pectoris) and mortality remain high despite treatment with ACE inhibitors. In the search for future improvements, the new generation of long-acting dihydropyridines is worth considering. Their afterload reducing action, coupled with powerful coronary vasodilation, might hypothetically delay the progression of ischemic LV dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1977

Reversal of advanced left ventricular dysfunction following aortic valve replacement for aortic stenosis.

A series of 12 consecutive patients who underwent aortic valve replacement (AVR) for aortic stenosis complicated by severe left ventricular dysfunction was reviewed. Ventricular dysfunction was reflected by pulmonary congestion, edema, renal and hepatic dysfunction, and by severely depressed ejection fractions (mean, 13%; range equal to 0-20%). Aortic valve replacement was accompanied by mitral commissurotomy in 1 patient and aortocoronary bypass in 5. Three of 5 patients with greater than 50% coronary obstruction died without reversal of heart failure, and 1 of the 5 died after a stroke. The 1 survivor of this group has done well. All 7 patients with minimal or no coronary disease survived operation and are now in New York Heart Association Class I or II. Postoperative catheterization (2 to 12 months) in 6 patients showed improved cardiac index and filling pressures. Left ventricular diastolic volume fell from 159 to 82 ml/m2, and ejection fraction rose from 13 to 45%. We conclude that left ventricular dysfunction owing to aortic stenosis alone is reversible and that AVR results in great clinical improvement. When coronary disease is present, survival may be accompanied by great improvement but the operative mortality is much higher.

Aged↗

PubMed1994

Heart rate variability in left ventricular dysfunction and heart failure: effects and implications of drug treatment.

OBJECTIVE: To review the importance of heart rate variability analysis in left ventricular dysfunction and heart failure and to assess the effects of drug treatment. In patients with left ventricular dysfunction or heart failure, a low heart rate variability is a strong predictor of a low probability of survival. Because drug treatment in these patients has rapidly changed over the past two decades, the effect of these drugs on heart rate variability needs special attention. DESIGN: A study of published reports to give an overview of heart rate variability in patients with left ventricular dysfunction or heart failure and how it is affected by drug treatment. RESULTS: Analysis of heart rate variability provides an easily obtained early marker for progression of disease. It seems to be more closely related to the degree of neurohumoral activation than to haemodynamic variables. Cardiovascular drugs may either stimulate or inhibit the degree of neurohumoral activation, and the effects of pharmacological intervention can be closely monitored with this method. CONCLUSIONS: The analysis of heart rate variability, including spectral analysis, is a novel non-invasive way to obtain potentially useful clinical information in patients with reduced left ventricular function. The effects of drug treatment on heart rate variability are in general consistent with their long-term effects in left ventricular dysfunction and heart failure.

Heart Failure↗

PubMed2004

[Relationship between coronary flow reserve and recovery of regional left ventricular function in patients with tako-tsubo-like transient left ventricular dysfunction].

OBJECTIVES: This study assessed the relationship between coronary flow reserve and functional recovery of left ventricular wall motion in patients with tako-tsubo-like transient left ventricular dysfunction. METHODS: Coronary flow reserve was measured using the Doppler guide wire technique in the left descending coronary artery in nine consecutive patients (three men, six women, mean age 71 +/- 11 years) with tako-tsubo-like transient left ventricular dysfunction. Regional wall motion was analyzed to estimate anterior wall motion score index (anterior WMSI) by transthoracic echocardiography on admission and 3 weeks after the onset of symptoms. RESULTS: Anterior WMSI was 2.2 +/- 0.4 on admission and improved to 1.4 +/- 0.5 at 3 weeks later (p < 0.001). Coronary flow reserve on admission was not correlated to the anterior WMSI on admission (r = 0.19, p = 0.63). However, coronary flow reserve on admission was correlated to the improvement in anterior WMSI (r = 0.74, p = 0.02). CONCLUSIONS: Coronary microcirculation is damaged in acute phase of tako-tsubo-like transient left ventricular dysfunction. The severity of coronary microvascular dysfunction influences the degree of left ventricular wall motion recovery.

Aged↗