SEARCH · PubMed Health

Results for “Ventricular Dysfunction, Left”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 199 records · Page 11Linked to original sources

PubMedDate not supplied

Usefulness of distinct activity thresholds according to baseline regional asynergy for predicting functional recovery in patients with chronic coronary artery disease and left ventricular dysfunction: a study with nitrate-enhanced sestamibi gated SPECT.

BACKGROUND: The role of gated single photon emission computed tomography (SPECT) in improving viability detection with the use of perfusion imaging is uncertain. This study aimed to verify whether the classification of baseline regional dysfunction with gated SPECT helps to predict functional recovery with the use of quantitative perfusion imaging. METHODS AND RESULTS: Resting nitrate-enhanced sestamibi gated SPECT was performed in 31 patients with left ventricular dysfunction, who later underwent coronary revascularization. With the use of a 16-segment model, tracer activity was quantified, and wall motion and thickening were estimated with a 4-point scoring scheme. Reversible dysfunction was assessed with follow-up gated SPECT. According to receiver operating characteristic curve analysis, the best overall cutoff for predicting reversible dysfunction in asynergic segments was 50% of peak activity or greater, with 83% sensitivity, 54% specificity, and 64% accuracy. When the segments were divided according to wall motion in resting gated SPECT, the optimal activity cutoff was greater than 68% for hypokinetic and 50% or greater for adyskinetic segments. With the use of 2 thresholds, the overall sensitivity remained good (76%), whereas specificity increased to 73% (P <.0005) and accuracy to 74% (P <.02). CONCLUSIONS: Regional dysfunction assessment directly on perfusion images permits use of different activity thresholds with an improvement over a single cutoff for all asynergic segments. Therefore combining perfusion and functional data with nitrate-enhanced gated SPECT at rest appears to be a promising approach for viability detection.

Adult↗

PubMed1999

Angiotensin-converting enzyme inhibition facilitates alveolar-capillary gas transfer and improves ventilation-perfusion coupling in patients with left ventricular dysfunction.

OBJECTIVE: The backward effects of left ventricular dysfunction include alterations in alveolar-capillary gas transfer and ventilation-perfusion coupling. Because the angiotensin-converting enzyme (ACE) is highly concentrated in the vascular endothelium of the lungs, we examined whether ACE inhibitors may influence the pulmonary function in patients with congestive heart failure. METHODS: In 20 patients with idiopathic cardiomyopathy, pulmonary function and exercise capacity were evaluated at baseline and 6 and 12 months after treatment with enalapril (10 mg twice a day) was started. The study also included 19 age- and sex-matched control subjects with mild primary hypertension and normal left ventricular function who were given enalapril as a standard treatment of high blood pressure. RESULTS: In congestive heart failure, forced expiratory volume in 1 second, vital capacity, and total lung capacity did not vary significantly with enalapril; alveolar-capillary diffusion of carbon monoxide (DL(CO)) increased toward normal; exercise tolerance time, peak exercise oxygen uptake (peak VO2), minute ventilation and tidal volume (peak VT) also increased; and the ratio of volume of dead space (VD) to VT (peak VD/VT) at peak exercise reduced. Changes in peak VO2 showed a direct correlation with those in DL(CO) and an inverse correlation with those in peak VD/VT. Results at 6 and 12 months were comparable. Enalapril did not affect these variables in the control population. CONCLUSIONS: In patients with idiopathic cardiomyopathy heart failure, but not in control subjects, gas transfer and ventilation-perfusion improved with ACE inhibition. These pulmonary changes may contribute to the associated increase in exercise tolerance.

Adult↗

PubMed2004

Non-ischemic left ventricular dysfunction after pediatric cardiac transplantation: treatment with plasmapheresis and OKT3.

BACKGROUND: Acquired left ventricular dysfunction after pediatric cardiac transplantation is associated with a high mortality rate. It often occurs without biopsy evidence of cellular rejection or severe transplant coronary arteriopathy. METHODS: We employed a protocol for treatment of acquired, non-ischemic left ventricular dysfunction utilizing plasmapheresis, monoclonal anti-T-cell antibody (OKT3), cyclophosphamide and steroids, regardless of the results of endomyocardial biopsy. Left ventricular dysfunction was defined as an echocardiographic shortening fraction of <29% and/or symptoms of congestive heart failure requiring inotropic support. Transplant coronary arteriopathy was excluded by coronary angiography in all cases. RESULTS: Ten pediatric heart transplant recipients were treated for 13 episodes of non-ischemic left ventricular dysfunction. Biopsy scores were low grade (ISHLT Grade 1A or 1B) in 8 episodes. Eight of 10 patients had a history of non-compliance in regularly taking immunosuppressant medications. Inotropic support was required in 9 of 13 cases, with a median duration of 5 days. Median left ventricular shortening fraction was 17% at time of presentation. Normalization of shortening fraction occurred a median of 40 days from the start of treatment. Survival to hospital discharge occurred in 11 of 13 (85%) patients. Long-term patient survival, however, was only 50% at 24 months after presentation with a first episode of acquired left ventricular dysfunction. CONCLUSIONS: Use of plasmapheresis, OKT3, cyclophosphamide and steroids resulted in successful short-term reversal of non-ischemic left ventricular dysfunction in pediatric heart transplant patients, but long-term survival remained poor.

Adolescent↗

PubMed2006

Prosthesis-patient mismatch after aortic valve replacement predominantly affects patients with preexisting left ventricular dysfunction: effect on survival, freedom from heart failure, and left ventricular mass regression.

OBJECTIVE: The effect of prosthesis-patient mismatch on clinical outcome and left ventricular mass regression after aortic valve replacement remains controversial. Data on whether the clinical effect of prosthesis-patient mismatch depends on left ventricular function at the time of aortic valve replacement are lacking. This study examined the long-term clinical and echocardiographic effects of prosthesis-patient mismatch in patients with and without left ventricular systolic dysfunction at the time of aortic valve replacement. METHODS: Preoperative and serial postoperative echocardiograms were performed in 805 adults who underwent aortic valve replacement between 1990 and 2003 and who were subsequently followed up in a dedicated valve clinic (follow-up, mean +/- SD, 5.5 +/- 3.5 years; maximum, 14.2 years). Preoperative left ventricular function was defined as normal (ejection fraction > or =50%) in 548 patients and impaired (ejection fraction <50%) in 257 patients. RESULTS: Patients with impaired preoperative left ventricular function and prosthesis-patient mismatch (indexed effective orifice area < or =0.85 cm2/m2) had a decreased overall late survival (hazard ratio, 2.8; P = .03), decreased freedom from heart failure symptoms or heart failure death (odds ratio of 5.1 at 3 years after aortic valve replacement; P = .009), and diminished left ventricular mass regression compared with patients with impaired preoperative left ventricular function and no prosthesis-patient mismatch. These effects of prosthesis-patient mismatch were not observed in patients with normal preoperative left ventricular function. CONCLUSIONS: Prosthesis-patient mismatch at an indexed effective orifice area of 0.85 cm2/m2 or less after aortic valve replacement primarily affects patients with impaired preoperative left ventricular function and results in decreased survival, lower freedom from heart failure, and incomplete left ventricular mass regression. Patients with impaired left ventricular function represent a critical population in whom prosthesis-patient mismatch should be avoided at the time of aortic valve replacement.

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

Reproducible model of post-infarction left ventricular dysfunction: haemodynamic characterization by conductance catheter.

OBJECTIVE: The understanding of pathophysiology and cellular mechanisms of chronic heart failure requires the creation of appropriate and accurately characterized animal models, thus enabling meaningful evaluation of evolving medical and surgical therapies. METHODS: The left anterior descending and its diagonal branch were ligated in 12 sheep to induce left ventricular dysfunction. RESULTS: Study of left ventricular pressure-volume loops 3 months post-operatively showed a significant deterioration of both systolic and diastolic indexes of left ventricular function. The left ventricular end-diastolic pressure increased from 3+/-1 to 7+/-1 mmHg (P<0.001) along with a substantial increase in end-diastolic volume from 78+/-8 to 121+/-6 ml (P=0.002) and a significant decrease in cardiac output from 2+/-0.2 to 1.5+/-0.2 l/min (P=0.001). The left ventricular end-systolic pressure-volume relationship deteriorated from 2.7+/-0.37 to 0.7+/-0.16 mmHg/ml (P=0.0002) along with a significant reduction in the pre-load recruitable stroke work (P=0.001). The ejection fraction decreased from 34+/-2% to 16+/-4% (P<0.001) with a significant decrease in +dp/dt and -dp/dt (P=0.009). The mean systemic blood pressure, however, was maintained due to a substantial increase in the systemic vascular resistance (P=0.007). CONCLUSION: This study describes a reproducible large animal model of left ventricular dysfunction. This model is potentially useful to study the pathogenesis of remodelling, surgical management of heart failure and development of novel treatment strategies.

Animals↗

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↗

PubMed2004

Brain natriuretic peptide and left ventricular dysfunction in chagasic cardiomyopathy.

Global left ventricular (LV) systolic dysfunction is the strongest predictor of morbidity and mortality in Chagas disease. Echocardiography is considered the gold standard for the detection of LV dysfunction, but not always available in endemic areas where chagasic cardiomyopathy is most common. Brain natriuretic peptide (BNP) is a neurohormone that has been recently described as a simple and inexpensive diagnostic and prognostic marker for patients with congestive heart failure. Chagasic patients (n = 63) and non-infected healthy individuals (n = 18) were recruited prospectively and underwent complete clinical examination, echocardiography and 24-h Holter monitoring. BNP was measured from thawed plasma samples using the Triage BNP test. We observed high levels of BNP in association with depression of LV ejection fraction, with increase of LV end-diastolic diameter and with LV premature complexes. An elevated concentration of BNP, defined as a concentration of 60 pg/ml or more, had a sensitivity of 91.7%, specificity of 82.8%, positive predictive value of 52.4%, and negative predictive value of 98% for detecting LV dysfunction (LV ejection fraction < 40%).BNP measurement using a simple, relatively inexpensive and rapid test has a promising role in identifying LV dysfunction associated with chagasic cardiomyopathy. Equally important, patients with Trypanosoma cruzi infection who have low levels of BNP level in plasma have a very low likelihood of severe cardiac involvement, and echocardiography is probably not necessary.

Adult↗

PubMed1995

Reversible left ventricular dysfunction associated with Guillain-Barré syndrome--an expression of catecholamine cardiotoxicity?

The patient was a 76-year-old female who had a history of Guillain-Barré syndrome 3 years previously; ST-segment elevation was noted in association with reversible left ventricular dysfunction. Left ventrioculogram and coronary angiograms were normal and ergonovine test was negative during the chronic period of Guillain-Barré syndrome. She was hospitalized again due to the recurrence of Guillain-Barré syndrome. Two days later, ST-segment elevation in leads V2 through V5 prompted us to perform cardiac catheterization, although she did not complain of any chest symptoms. A large akinetic area was found mainly around the apex on left ventriculography, despite the lack of coronary stenoses. Peak creatine kinase and C-reactive protein were 400 IU/ml and 3.5 mg/dl, respectively. Left ventricular dysfunction was normalized within one week. During the acute phase of the cardiac episode, plasma norepinephrine and epinephrine were 1340 pg/ml and 112 pg/ml, respectively. I123 metaiodobenzyl-guanidine myocardial scintigram 3 weeks after the episode showed an extensive apical defect which was improved markedly 3 months later. We think that this reversible left ventricular dysfunction was due to the synergistic toxic effect of mildly increased catecholamine and transiently damaged sympathetic nerve endings in the myocardium, presumably due to Guillain-Barré syndrome.

3-Iodobenzylguanidine↗

PubMed1999

An immunoluminometric assay for N-terminal pro-brain natriuretic peptide: development of a test for left ventricular dysfunction.

Measurement of plasma levels of brain natriuretic peptide (BNP) has been used to assess left ventricular dysfunction and prognosis. Levels of the N-terminus of the precursor of BNP (NT-proBNP) have been reported to be elevated to a greater extent than BNP in left ventricular dysfunction. We have devised a non-radioactive sensitive and specific assay for NT-proBNP based on a competitive ligand binding principle. The chemiluminescent label 4-(2-succinimidyloxycarbonylethyl)phenyl-10-methylacridinium 9-carboxylate fluorosulphonate was used to label peptides representing domains in the middle and C-terminal sections of NT-proBNP. Assay of the C-terminal section of NT-proBNP (amino acids 65-76) in patients with proven left ventricular dysfunction [left ventricular wall motion index median 0.9 (range 0.3-1.4)] revealed elevated values [median 639 (386-911) fmol/ml] compared with normal controls [left ventricular wall motion index of 2 in all, NT-proBNP median 159 (120-245) fmol/ml, P<0.001]. Measurement of the middle section of NT-proBNP (amino acids 37-49) was not a discriminating test. It is thus possible to derivatize small peptides with a methyl acridinium label and preserve immunodetection with specific antibodies. Such methodology may allow non-radioactive immunoluminometric assays to be devised.

Adult↗

PubMed1999

[Dobutamine doppler echocardiography in severe aortic stenosis with left ventricular dysfunction. Comparison with postoperative examination].

The association of left ventricular dysfunction with aortic stenosis worsens the spontaneous prognosis and increases operative mortality. The aim of this prospective study was to assess the predictive value of dobutamine Doppler echocardiography on the indices of left ventricular contractile function in patients with aortic stenosis and left ventricular dysfunction (LVEF < 0.45) undergoing aortic valve replacement. Eighteen patients, including 9 with coronary artery disease, were included in a protocol consisting of analysis of left ventricular function and of the severity of aortic stenosis before, during dobutamine infusion, and after valvular replacement. The dobutamine was given in progressive increments of 5 micrograms/Kg up to a maximum of 20 micrograms/Kg. During pharmacological stress, the functional aortic valve area increased from 0.46 +/- 0.15 to 0.56 +/- 0.23 cm2. Tolerance of the procedure was good. All but 2 patients improved their postoperative ejection fraction with values equivalent to those observed during the last increment of dobutamine (r = 0.73; p < 0.003). The patients with initial mean pressure gradients > 50 mmHg normalised their LVEF after valve replacement. The authors conclude that dobutamine echocardiography is useful for predicting the values of postoperative left ventricular contractile indices when severe aortic stenosis is associated with systolic dysfunction. It allows evaluation of the expected short term benefits to these indices after aortic valve replacement.

Adult↗

PubMed2002

CD14-deficient mice are protected against lipopolysaccharide-induced cardiac inflammation and left ventricular dysfunction.

BACKGROUND: The molecular mechanisms responsible for sepsis-induced myocardial dysfunction remain undefined. CD14 mediates the inflammatory response to lipopolysaccharide (LPS) in various organs including the heart. In this study we investigated the role of CD14 in LPS-induced myocardial dysfunction in vivo. METHODS AND RESULTS: Wild-type and CD14-deficient (CD14-D) mice were challenged with Escherichia coli LPS. Myocardial tumor necrosis factor, interleukin-1beta (IL-1beta), and NOS2 induction was measured before and 6 hours after LPS challenge. Echocardiographic parameters of left ventricular function were measured before and 6 hours after LPS administration. LPS challenge induced a significant increase in myocardial tumor necrosis factor and IL-1beta mRNA and protein expression in wild-type mice. In contrast, mRNA and protein levels for TNF and IL-1beta were significantly blunted in CD14-D mice. An increase in NOS2 protein was noted within 6 hours of LPS provocation only in the hearts of wild-type mice. This was associated with an increase in ventricular cGMP levels. Activation of nuclear factor-kappaB was observed within 30 minutes of LPS in the hearts of wild-type mice but not in CD14-D mice. In wild-type mice, LPS significantly decreased left ventricular fractional shortening, velocity of circumferential shortening, and dP/dt(max). LPS-treated CD14-D mice maintained normal cardiac function. CONCLUSIONS: These results suggest that CD14 is important in mediating the proinflammatory response induced by LPS in the heart and that CD14 is necessary for the development of left ventricular dysfunction during LPS-induced shock in vivo.

Animals↗

PubMed2006

Triggers of sustained monomorphic ventricular tachycardia differ among patients with varying etiologies of left ventricular dysfunction.

BACKGROUND: The mechanisms underlying the initiation of sustained ventricular tachycardia (VT) have not been fully elucidated. The extent to which reentry, abnormal automaticity, and triggered activity play a role in VT differs depending on the etiology of left ventricular dysfunction. By analyzing electrograms from implantable cardioverter defibrillator (ICD), we sought to determine whether there were differences in VT initiation patterns between patients with ischemic and nonischemic cardiomyopathy. METHODS: We analyzed ICD electrograms in patients with ejection fractions < 40% who had sustained VT over a 27-month period. The trigger for VT onset was classified as a ventricular premature beat (VPB), supraventricular tachycardia, or of "sudden onset." The baseline cycle length, VT cycle length, coupling interval, and prematurity ratio were recorded for each event. The prematurity ratio was calculated as the coupling interval of the VT initiator divided by the baseline cycle length. RESULTS: Sixty-three VT events in 14 patients met the inclusion criteria. A VPB initiated the VT in 58 episodes (92%), 1 episode (2%) was initiated by a supraventricular tachycardia, and 4 episodes (6%) were sudden onset. The prematurity ratio was significantly higher (P < 0.05) in patients with ischemic cardiomyopathy (0.751 +/- 0.068) as compared to patients with nonischemic cardiomyopathy (0.604 +/- 0.139). CONCLUSION: VPBs initiated most sustained VT episodes. A significantly higher prematurity ratio was observed in the ischemic heart disease group. This may represent different mechanisms of VT initiation in patients with ischemic versus nonischemic heart disease.

Aged↗

PubMed1980

Exercise capacity in patients with severe left ventricular dysfunction.

Normal or near-normal exercise capacity has been thought to reflect normal left ventricular function. Many compensatory mechanisms could preserve exercise capacity in patients with severe left ventricular dysfunction. We evaluated exercise capacity using a treadmill exercise test in 26 patients with severe left ventricular dysfunction defined by a left ventricular ejection fraction of 30% or less by isotope ventriculography. One half of the patients had normal exercise capacity and a normal cardiothoracic ratio on chest x-ray. This study indicates that traditional predictors of left ventricular function that have been widely used in clinical evaluation of the patients with cardiac disease (cardiothoracic ratio and exercise capacity) can be normal in a significant number of patients with severe left ventricular dysfunction. Thus, left ventricular function cannot be accurately estimated using these traditional predictors and should be assessed quantitatively. The isotope ventriculogram appears to be ideal for this purpose.

Adult↗

PubMed2002

Normal coronary arteries and isolated, regional, left ventricular dysfunction in myotonic dystrophy: a case report.

Development of cardiomyopathy in myotonic dystrophy is rare. Regional ventricular abnormality in the presence of normal coronary vessels has not been reported in this condition. We describe a case of isolated, regional, left ventricular dysfunction with corresponding defects on nuclear perfusion imaging in a patient with classical myotonic dystrophy and normal coronary arteries.

Adult↗

PubMed2001

Prediction of long-term outcomes by signal-averaged electrocardiography in patients with unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction.

BACKGROUND: An abnormal signal-averaged ECG (SAECG) is a noninvasive marker of the substrate of sustained ventricular tachycardia after myocardial infarction. We assessed its prognostic ability in patients with asymptomatic unsustained ventricular tachycardia, coronary artery disease, and left ventricular dysfunction. METHODS AND RESULTS: A blinded core laboratory analyzed SAECG tracings from 1925 patients in a multicenter trial. Cox proportional hazards modeling was used to examine individual and joint relations between SAECG variables and arrhythmic death or cardiac arrest (primary end point), cardiac death, and total mortality. We also assessed the prognostic utility of SAECG at different levels of ejection fraction (EF). A filtered QRS duration >114 ms (abnormal SAECG) independently predicted the primary end point and cardiac death, independent of clinical variables, cardioverter-defibrillator implantation, and antiarrhythmic drug therapy. With an abnormal SAECG, the 5-year rates of the primary end point (28% versus 17%, P=0.0001), cardiac death (37% versus 25%, P=0.0001), and total mortality (43% versus 35%, P=0.0001) were significantly higher. The combination of EF <30% and abnormal SAECG identified a particularly high-risk subset that constituted 21% of the total population. Thirty-six percent and 44% of patients with this combination succumbed to arrhythmic and cardiac death, respectively. CONCLUSIONS: SAECG is a powerful predictor of poor outcomes in this population. The noninvasive combination of an abnormal SAECG and reduced EF may have utility in selecting high-risk patients for intervention.

Coronary Disease↗

PubMed1999

Trandolapril reduces the incidence of atrial fibrillation after acute myocardial infarction in patients with left ventricular dysfunction.

BACKGROUND: Studies have suggested that ACE inhibitors have an antiarrhythmic effect on ventricular arrhythmias. Whether they have an effect on atrial fibrillation is unknown. METHODS AND RESULTS: We investigated the effect of ACE inhibition with trandolapril on the incidence of atrial fibrillation in patients with reduced left ventricular function secondary to acute myocardial infarction. The patients in this study were those who qualified for inclusion into the TRAndolapril Cardiac Evaluation (TRACE) study, a randomized double-blind placebo-controlled study and who had sinus rhythm on the ECG obtained at randomization. Patients who fulfilled the criteria for inclusion were randomized to treatment with the ACE inhibitor trandolapril or placebo and were followed up for 2 to 4 years. Development and time to occurrence of atrial fibrillation in one 12-lead ECG recorded at the outpatient visits was the primary end point of this investigation. Of the 1749 patients included in the TRACE study, 1577 had sinus rhythm on the ECG recorded at randomization. Of these patients, 790 were randomized to trandolapril treatment and 787 to placebo treatment. The groups differed only slightly with respect to baseline characteristics. A total of 64 patients developed atrial fibrillation during the 2- to 4-year follow-up period. Significantly more patients developed atrial fibrillation in the placebo group than in the trandolapril group, 5.3% (n=42) versus 2.8% (n=22), respectively, P<0.05. Cox multivariable regression analysis, adjusting for important baseline characteristics, revealed that trandolapril treatment significantly reduced the risk of developing atrial fibrillation (RR, 0.45; 95% CI, 0.26 to 0.76; P<0.01). CONCLUSIONS: The results from the present study demonstrate that trandolapril treatment reduces the incidence of atrial fibrillation in patients with left ventricular dysfunction after acute myocardial infarction.

Aged↗

PubMed2005

Usefulness of latent left ventricular dysfunction assessed by Bowditch Treppe to predict stress-induced pulmonary hypertension in minimally symptomatic severe mitral regurgitation secondary to mitral valve prolapse.

We assessed whether the presence of latent myocardial dysfunction, evaluated by echocardiographic derived force-frequency relationship (FFR) during exercise, predicts the appearance of stress-induced pulmonary hypertension in minimally symptomatic patients with severe mitral regurgitation (MR). Two groups of patients were identified: group I with normal (</=40 mm Hg) and group II with abnormal (>40 mm Hg) peak stress systemic pulmonary artery pressure. Group I had normal and upsloping FFR and group II had abnormal flat or biphasic FFR. Therefore, in patients with severe MR and apparently normal left ventricular function, the stress-induced pulmonary hypertension seems to be related to the presence of latent left ventricular dysfunction.

Analysis of Variance↗