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Left ventricular dysfunction discriminated noninvasively beat by beat.

To discriminate left ventricular (LV) dysfunctional beats noninvasively, simultaneous systolic time intervals (STI), acceleration ballistocardiograms (BCG) and respiratory cycle were recorded in 102 men with no history of cardiac disease and in 20 men with proved myocardial infarction or systemic hypertension. Thirty-six measurements were made on each heartbeat on a maximum of 20 beats per patient. The ratio of preejection period to LV ejection time (ET) varied significantly with the respiratory cycle in normal men, but not in men with proved myocardial infarctions or systemic hypertension. The BCG I-wave amplitude varied significantly with respiration in all 3 groups. Various statistical methods identified 9 primary variables of the 36, which differed significantly in a training group of 275 heartbeats in 19 normal, vs 46 beats in 5 coronary patients. A nonlinear quadratic discriminant function based on these primary variables identified 87% of the heartbeats as "normal" in the normal men and 98% as "coronary" in the coronary men. A test group of normal men older than 40 years showed 89% of 97 heartbeats "normal" and in hypertensive men 67% of 85 beats "normal." Comparison by patients showed a range of "coronary" beats in the training normal group from 0 to 50%, the older normal group 0 to 33%, and in the hypertensive patients 0 to 88%. The appropriate use of quadratic discriminant analysis to multivariable data may yield information not otherwise seen. A beat-by-beat identification of dysfunctional beats at rest may lead to a sensitive index that is prognostically useful.

Adult↗

Hemodynamic and myocardial metabolic effects of the beta-agonist prenalterol in ischemic left ventricular dysfunction.

Hemodynamic and myocardial metabolic parameters in ischemic left ventricular (LV) dysfunction were evaluated in response to the beta-agonist prenalterol. Twenty micrograms/kg intravenous prenalterol increased resting heart rate and cardiac output and decreased LV filling pressure, systemic vascular resistance, and pulmonary artery pressure. Resting coronary blood flow and myocardial oxygen consumption increased but net myocardial lactate and oxygen extraction did not change significantly. During pacing induced tachycardia (121 +/- 4 beats/min), prenalterol improved cardiac index and stroke work index; whereas, LV filling pressure, systemic vascular resistance, and pulmonary artery pressure decreased. Coronary blood flow and myocardial oxygen extraction did not change significantly. Net myocardial lactate extraction during pacing decreased insignificantly; one patient developed overt lactate production. Thus, prenalterol improves cardiovascular function at rest and during pacing-induced tachycardia in ischemic LV failure, but at the cost of higher resting myocardial oxygen consumption. The majority of subjects had no adverse metabolic response.

Adrenergic beta-Agonists↗

Reversal of left ventricular dysfunction following ablation of atrial fibrillation.

BACKGROUND: Evaluation of ventricular rate control in atrial fibrillation (AF) can be difficult, and the presence of an AF-induced ventricular cardiomyopathy due to intermittent poor rate control or other causes may be underestimated. The outcome with AF ablation in patients with a decreased left ventricular ejection fraction (LVEF) may provide insight into this important clinical issue. OBJECTIVE: To determine the effect of pulmonary vein isolation on LVEF in patients with AF and decreased LVEF (< or = 50%). METHODS: Ablation consisted of proximal isolation of arrhythmogenic pulmonary veins (PVs) and elimination of non-PV triggers. LVEF was determined within 24 hours after ablation and again at up to 6 months follow-up. Transtelephonic monitoring was performed routinely for 2-3 weeks prior to ablation, at 6 weeks, and 6 months post and with symptoms following ablation. AF control was defined as freedom from AF or marked (>90%) reduction in AF burden on or off previously ineffective antiarrhythmic medication. RESULTS: AF ablation was performed in 366 patients and 67 (18%) patients had decreased LV function with a mean LVEF of 42 +/- 9%. An average of 3.4 +/- 0.9 PVs were isolated. AF control in the depressed LVEF group compared favorably with the normal EF group (86% vs. 87% P = NS), although more redo procedures were required (1.6 +/- 0.8 vs 1.3 +/- 0.6 procedures; P < or = 0.05). Only 15 of 67 patients (22%) with decreased LVEF had shown tachycardia (>100 bpm) on repeated preablation ECG recordings during AF. In the decreased LVEF group, the LVEF increased from 42 +/- 9% to 56 +/- 8% (P < 0.001) after ablation. CONCLUSIONS: Patients with AF and decreased LVEF undergoing AF ablation have similar success to patients with normal LVEF and have improvement in LVEF after ablation. These results suggest the presence of a reversible AF-induced ventricular cardiomyopathy in many patients with AF and depressed LV function. The presence of under-recognized and reversible cardiomyopathy even when tachycardia is not persistent is important to recognize.

Atrial Fibrillation↗

[Diastolic left ventricular dysfunction with microvascular angina (Syndrome X)].

Findings on left ventricular function in microvascular angina (syndrome X) are somewhat controversial. Recently, an increased prevalence of insulin resistance and hyperlipoproteinemia has been demonstrated as well as arterial hypertension potentially impairing the left ventricular diastolic function. In an attempt to analyze the diastolic function at rest, we investigated by Doppler echocardiography the transmitral blood flow in 16 patients (51 +/- 8 years). The diastolic data were compared with those of 12 healthy people (50 +/- 6 years) who were matched for age. The patients with microvascular angina revealed a slightly higher systolic blood pressure (134 +/- 18 mm Hg vs 125 +/- 9 mm Hg, n.s.), but imposed by higher left ventricular mass index (92 +/- 18 g/m2 vs 65 +/- 13 g/m2, p < 0.001). There was a trend to an elevated A-wave-peak during transmitral blood flow (61 +/- 14 cm/s vs 50 +/- 9 cm/s). The findings suggest impairment of the left ventricular relaxation before manifestation of left ventricular hypertrophy and hypertension takes place.

Adult↗

Atrial fibrillation as a cause of left ventricular dysfunction after cardiac transplantation.

We report 3 cases of late-onset atrial fibrillation several years after cardiac transplantation, each involving left ventricular systolic dysfunction in the absence of cardiac rejection or cardiac allograft vasculopathy. Although the etiology of late-onset atrial fibrillation in cardiac transplant recipients is not clear, its presence in the absence of cardiac rejection or coronary allograft vasculopathy can result in left ventricular systolic dysfunction, and therefore should be considered in the differential diagnosis of cardiac allograft failure. The onset of atrial fibrillation years after a heart transplant is not necessarily an indication of rejection. Aggressive rate control and restoration of normal sinus rhythm may improve allograft function in such cases.

Atrial Fibrillation↗

Effects of chronic administration of a vasopressin antagonist with combined antivasopressor and antiantidiuretic activities in rats with left ventricular dysfunction.

The present experiments were designed to study the long-term aquaretic effect of [d(CH2)5-D-Tyr(Et)VAVP], an antagonist to arginine vasopressin (AVP) with combined vascular (V1) and renal (V2) receptor inhibiting properties, in rats with left ventricular dysfunction resulting from myocardial infarction (MI). The continuous intravenous infusion of the AVP antagonist (36 micrograms/12 microliters/day) via osmotic minipumps over 11 days resulted in an increase in urine volume and a decrease in urinary osmolality by approximately 10-fold on the first day, but in subsequent days this response decreased in both the post-MI (n = 7) and normal (n = 6) rats. Nevertheless, the daily urine volume remained significantly higher and the urinary osmolality lower in the post-MI rats than in the normal ones throughout the study (p less than 0.05). In two other groups of post-MI (n = 5) and normal (n = 6) rats, intermittent intraperitoneal injections of the AVP antagonist (100 micrograms/kg) every third day resulted in a profound diuresis that was reproducible by each injection and was again significantly greater in the post-MI rats than in the normal rats (p less than 0.05). The cumulative urinary output over the first 10-day period of each treatment was greater with intermittent injections than with continuous infusion in both the post-MI and normal rats, but the difference was significant only in the post-MI rats (398.82 +/- 12.87 ml vs 309.07 +/- 32.44 ml, intermittent vs continuous, respectively, p less than 0.05), even though the cumulative dose of AVP antagonist given intermittently was only about one third of that given continuously.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Determinants of variable exercise performance among patients with severe left ventricular dysfunction.

The relation between bicycle exercise performance and determinants of central and peripheral cardiovascular function was assessed in 17 patients with class II to III heart failure and in 9 normal subjects. Proportional changes in oxygen consumption (VO2) from rest (R) to maximal exercise (Ex), or Mets, were used as an objective measure of the exercise capacity or functional reserve of the cardiovascular system. Left ventricular ejection fraction (EF) and proportional changes in end-diastolic volume, stroke volume, and cardiac output were determined from appropriate count data by equilibrium radionuclide angiography. Proportional changes in arteriovenous oxygen difference (A-VO2) were derived from the equation Ex/R A-VO2 = Ex/R VO2 divided by Ex/R CO, where CO = count output. Each subject exercised to an anaerobic endpoint. Maximal VO2 was significantly lower in patients than in normal subjects. Because Ex/R A-VO2 was comparable in normal subjects and patients, the lower exercise performance in patients resulted from a reduced count output response. The reduced CO response in patients resulted from failure of the ejection fraction to increase or from an attenuated heart rate response, or both. Exercise performance was variable in both groups. Multivariable analysis in the patient group identified changes in heart rate, count output, and A-VO2 with exercise as important predictors of Mets, but found no relation between Mets and changes in ejection fraction or stroke counts during exercise. Similarly, multiple regression analyses between Mets and determinants of cardiovascular function demonstrated significant correlations with Ex/R heart rate, Ex/R count output, and Ex/R A-VO2 in both groups. In patients, EF at rest ranged from 0.09 to 0.36, but it did not correlate with Mets, nor did changes in ejection fraction, stroke counts, or end-diastolic counts during exercise. The variable exercise performance among patients with severe left ventricular dysfunction was determined predominantly by a variable heart rate and A-VO2 response and not by rest or exercise indexes of left ventricular function.

Adult↗

Persistent hyperglycemia is associated with left ventricular dysfunction in patients with acute myocardial infarction.

BACKGROUND: The relationship of changes in blood glucose concentrations after admission to left ventricular (LV) dysfunction in patients with recanalized anterior acute myocardial infarction (AMI) remains unclear. METHODS AND RESULTS: Blood glucose concentrations were measured on admission and 24 h after symptom onset in 210 patients with recanalized anterior AMI within 6 h of symptom onset. Of them, 142 had hyperglycemia on admission, defined as a blood glucose >or=8.9 mmol/L, and 68 patients did not. Among the patients with admission hyperglycemia, 49 had persistent hyperglycemia, defined as a blood glucose >or=8.9 mmol/L 24 h after onset, and 93 did not. The incidences of myocardial blush grade of 0/1 after recanalization indicating impaired myocardial perfusion (71%), and peak creatine kinase concentration (5,631+/-2,855 mU/ml) were higher and predischarge LV function (43+/-11%) was lower in patients with persistent hyperglycemia than in those without (p<0.01). Multivariate analysis showed that persistent hyperglycemia was independently associated with LV dysfunction, defined as a predischarge LV ejection fraction <or=40% (odds ratio 7.38, p=0.001). CONCLUSIONS: Persistent hyperglycemia at 24 h after symptom onset is associated with LV dysfunction before discharge in patients with recanalized anterior AMI.

Adult↗

Dofetilide in patients with left ventricular dysfunction and either heart failure or acute myocardial infarction: rationale, design, and patient characteristics of the DIAMOND studies. Danish Investigations of Arrhythmia and Mortality ON Dofetilide.

BACKGROUND: Attempts to prolong life with antiarrhythmic drugs in patients at increased risk of sudden cardiac death have so far been disappointing or inconclusive. HYPOTHESIS: The Danish Investigations of Arrhythmia and Mortality ON Dofetilide (DIAMOND) encompass two survival studies testing the prophylactic use of the selective potassium-channel blocker, dofetilide, in patients at high risk of sudden death. METHODS: The first study includes patients admitted to hospital with congestive heart failure (CHF), the other includes patients with acute myocardial infarction (MI) within the previous 7 days. In both studies patients must have left ventricular systolic dysfunction (ejection fraction < or = 35%) determined by echocardiography. Each of the two studies are planned to enroll 1500 patients. Consecutive hospitalized patients with MI or CHF are screened in 37 Danish hospitals. Eligible patients are randomized to receive dofetilide or matching placebo. All patients are continuously monitored by telemetry for the first 3 days of the study to detect possible arrhythmic events and to ensure resuscitation in case of serious arrhythmias. Minimum duration of follow-up is 12 months. RESULTS: Between November 1993 and July 1996, a total of 5812 consecutive patients with CHF and 8688 consecutive patients with MI was screened for entry. Of these, 1518 patients were included in the CHF study and 1510 patients in the MI study. Overall 1-year mortality of randomized patients were 28 and 22%, respectively. CONCLUSION: DIAMOND will provide important data on the safety and efficacy of dofetilide in high-risk patients with left ventricular dysfunction and either CHF or MI, as well as evaluate tolerability in these populations.

Aged↗

Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator.

To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Salicylate reduces ventricular dysfunction and arrhythmias during reperfusion in isolated rat hearts.

Recent studies have shown the ability of salicylic acid (SA) to trap hydroxyl radicals (OH.) generated during reperfusion in ischemic myocardium. Since OH. is implicated in the pathogenesis of reperfusion injury, we examined the effect of SA on reperfusion-induced arrhythmias and postischemic ventricular dysfunction. Isolated rat hearts perfused by the Langendorff technique were preperfused with Krebs-Henseleit buffer containing SA for 10 min. Hearts were then made ischemic for 30 min, followed by 30 min of reperfusion. In a separate group, SA was administered only at the onset of reperfusion. The left ventricular contractile functions, left ventricular developed pressure (LVDP) and its first derivative (LV dP/dt), coronary flow (CF), and creatine kinase (CK) release were determined before and after ischemia. Epicardial electrocardiogram (ECG) was also recorded to analyze the incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF). SA improved LVDP, LV dp/dt, and CF recovery and reduced CK release compared to the control group. The incidence of VT and VF during reperfusion was also significantly reduced by SA. Analysis of tissue thiobarbituric acid-reactive products indicates that SA decreased oxidative stress during reperfusion. In conclusion, these results suggest that SA reduces myocardial reperfusion injury and attenuates ventricular arrhythmias by trapping OH. radicals upon reperfusion in isolated rat hearts.

Animals↗

Myocardial revascularization with bilateral internal thoracic artery in patients with left main disease or left ventricular dysfunction: an incremental risk?

Although long-term patency of the internal thoracic artery (ITA) is well stated, there is still some concern about its perioperative performance. We considered 122 consecutive patients, 63 with left main disease (LMD; mean age 60 years) and 59 with left ventricular dysfunction (LVD; mean age 59 years) who underwent coronary artery bypass grafting in our Institute from March 1988 to September 1992. Patients with LMD were divided into 2 groups: LMD I: 29 patients receiving only ITA grafts on the left coronary system and LMD II: 34 patients having a single ITA graft on the left coronary system. Patients with LVD were divided into: LVD I: 44 patients operated with bilateral ITA and LVD II: 15 patients receiving a single ITA graft. Perioperative complications in LMD I and LMD II patients were respectively: myocardial necrosis in 2 (6.9%) versus 3 (8.8%), use of intra-aortic balloon pump (IABP) in 2 (6.9%) versus 2 (5.9%); no death occurred in both groups. Perioperative results in groups LVD I and LVD II were: death in 1 patient (2.2%) versus 1 (6.7%), myocardial necrosis in 2 (4.5%) versus 1 (6.7%) and IABP in 4 (9.1%) versus 2 (13.3%). In our experience the use of bilateral ITA grafts in patients with LMD and LVD was not related to an incremental risk. We conclude that LMD and LVD should not be considered as contraindications to the extensive use of arterial conduits.

Aged↗

[99mTc-MIBI scintrigraphy for detecting viable myocardium in patients with previous infarction and ventricular dysfunction].

BACKGROUND: The detection of hibernating myocardium involved different imaging procedures, trying to predict the functional recovery of this tissue, which survives at a low metabolic rate in regions exposed to chronic ischemia. MATERIALS AND METHODS: A small group of patients with prior myocardial infarction and severe left ventricular dysfunction has been evaluated by echo-dobutamine and 99mTc-MIBI myocardial SPET. This radiopharmaceutical drug has been considered of low usefulness for the detection of viability. RESULTS AND CONCLUSIONS: By comparing scintigraphic and echographic results there seem to be a reduced probability of the presence of viable myocardium in regions with severe perfusional scintigraphic defect.

Aged↗

Nitrous oxide does not exacerbate pulmonary hypertension or ventricular dysfunction in patients with mitral valvular disease.

Using the rapid-response thermistor pulmonary artery catheter and transoesophageal echocardiography, this study examined the effects of 100 per cent oxygen, 70 per cent nitrous oxide/30 per cent oxygen, and 70 per cent nitrogen/30 per cent oxygen on the pulmonary circulation and ventricular function in ten patients with pulmonary hypertension. In comparison with baseline measurements, nitrous oxide administration resulted in small but statistically significant (P less than 0.05) changes in mean arterial pressure (76 +/- 14 to 67 +/- 12), mean pulmonary arterial pressure (37 +/- 14 to 33 +/- 13 mmHg), and cardiac output (3.7 +/- 1.4 to 3.2 +/- 1.1 L.min-1). Seventy per cent nitrogen resulted in no significant changes from baseline. The repeat 100 per cent oxygen measurements were nearly identical to the nitrous oxide measurements. It is concluded that nitrous oxide does not exacerbate pulmonary hypertension or ventricular dysfunction during high-dose fentanyl anaesthesia in patients with mitral valvular disease.

Adult↗

Atrial pacing induced left ventricular dysfunction: reversibility after aortocoronary bypass surgery.

Three patients with angina pectoris were studied before and after aortocoronary bypass surgery. Angiographic studies were performed with and without atrial pacing. Preoperative atrial pacing in all three patients resulted in angina and/or ST segment changes accompanied by regional left ventricular contractile abnormalities, decreased ejection fraction, as well as decreased left ventricular end-diastolic and stroke volumes. After surgery with all grafts patent, atrial pacing at similar heart rates did not produce an ischemic response. Left ventricular contractile pattern remained normal, and there was no change in ejection fraction though end-diastolic and stroke volumes decreased. These studies demonstrate that aortocoronary bypass surgery can abolish both the ischemic response and left ventricular dysfunction that accompany atrial pacing.

Angina Pectoris↗

Right ventricular dysfunction in acute thermal injury.

The elevated cardiac output (CO) and pulmonary artery hypertension (PAH) observed in thermal injury offers a unique opportunity to study the effects of a combined pressure-flow load on the right ventricle in previously healthy persons. Potential responses include a diminished right ventricular ejection fraction (RVEF), increased right ventricular end-diastolic volume index (RVEDVI), and augmented myocardial oxygen consumption because of increased systolic wall tension. We investigated these factors in 15 nonhypoxic patients without sepsis having 15--75% body surface area burns using flow directed catheters and the thermodilution technique. All patients increased their CO in response in fluid resuscitation, but six patients with an elevated mean pulmonary artery pressure (greater than 20 mmHG and increased pulmonary vascular resistance (greater than 1.2 mmHg/min/L) had right ventricular dysfunction as evidenced by an increase (188 +/- 15 ml/M2) in RVEDVI and a decreased (0.26 +/- 4 ml/M2) RVEF. Patients without PAH had a smaller RVEDVI (115 +/- 4 ML/M2) and larger RVEF (0.39 +/- 0.02). Patients with PAH and RV dysfunction were older, had larger body surface area burns, lower systemic diastolic artery pressures (63 +/- 4 mmHg) and higher heart rates (114 +/- 7 beats/min); RV end-diastolic pressures were minimally elevated (9.5 +/- 1.4 mmHg). The decrease in RVEF and increase in RVEDVI may limit the hemodynamic response to fluid volume replacement and survival.

Acute Disease↗

Metabolic evidence of viable myocardium in regions with reduced wall thickness and absent wall thickening in patients with chronic ischemic left ventricular dysfunction.

Reduced end-diastolic wall thickness with absent systolic wall thickening has been reported to represent nonviable myocardium in patients with chronic coronary artery disease. To assess whether reduced regional end-diastolic wall thickness and absent wall thickening accurately identify nonviable myocardium, 25 patients with ischemic left ventricular dysfunction (ejection fraction at rest 27 +/- 10%) underwent positron emission tomography with oxygen-15-labeled water and 18fluorodeoxyglucose to assess metabolic activity and spin-echo gated nuclear magnetic resonance imaging to measure regional end-diastolic wall thickness and wall thickening. The presence of metabolic activity was defined as 18fluorodeoxyglucose uptake (corrected for partial volume) greater than 50% of that in normal regions. Of 355 myocardial regions evaluated, 266 were hypokinetic or normokinetic at rest and 89 were akinetic (that is, absent wall thickening). 18Fluorodeoxyglucose uptake was observed in 97% of the hypokinetic and normokinetic regions and in 74% of the akinetic regions. End-diastolic wall thickness was greater in akinetic regions with than in those without 18fluorodeoxyglucose uptake (11 +/- 4 vs. 7 +/- 3 mm, p less than 0.01). The highest values for sensitivity and specificity of end-diastolic wall thickness in predicting the absence of metabolic activity in akinetic regions were 74% and 79%, respectively, and corresponded to an end-diastolic threshold of 8 mm. However, the positive predictive accuracy was only 55% and did not improve for other end-diastolic wall thickness values. In all myocardial regions, there was only a weak correlation between 18fluorodeoxyglucose activity and either end-diastolic wall thickness (r = 0.17) or wall thickening (r = 0.32). Thus, metabolic activity is present in many regions with reduced end-diastolic wall thickness and absent wall thickening. These data indicate that assessment of regional anatomy and function may be inaccurate in distinguishing asynergic but viable myocardium from nonviable myocardium.

Adult↗