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PubMed2006

Right ventricular dysfunction due to right ventricular outflow tract patch.

Doppler tissue imaging analysis was used to examine the relationship between right ventricular function and right ventricular outflow tract damage in 54 patients with repaired tetralogy of Fallot. The patients were divided into three groups: 16 in whom the right ventricular outflow tract was directly sutured (group DS), 23 who had transventricular patch repair (group TVP), and 15 who had transannular patch repair (group TAP). The control group consisted of 16 age-matched patients who underwent patch closure of a ventricular septal defect (group C). The Tei index was obtained from tricuspid and pulmonary Doppler flow velocities. The right ventricular Tei index was significantly greater in groups TVP and TAP than in group DS. Doppler tissue imaging analysis in groups TVP and TAP showed shorter myocardial systolic velocity, diastolic peak velocity, and atrial diastolic peak velocity, lower peak myocardial velocity and acceleration during isovolumic contraction, and prolonged isovolumic relaxation and contraction times compared to groups DS and C. Right ventricular dysfunction is due to the right ventricular outflow tract patch. Thus, the right ventricular outflow tract may be essential for right ventricular ejection and maintenance of right ventricular function.

Adolescent↗
PubMed1995

Use of electrophysiological studies in the diagnosis and treatment of cardiac patients with left ventricular dysfunction and high grade ventricular ectopy.

We studied the sudden death occurrence in 28 patients (23 males, age 59.2 +/- 15.6 years) who had a documented cardiac disease with left ventricular dysfunction (ejection fraction < or = 0.4) and high grade ventricular ectopy. None had suffered from spontaneous sustained ventricular arrhythmia and/or syncope. Their diagnosis and treatment were guided by electrophysiological studies. Electrophysiological studies were performed in the antiarrhythmic drug-free state. In cases when sustained ventricular arrhythmias could be induced, antiarrhythmic treatment was prescribed according to the results of the electrophysiological studies. In cases of non-inducibility, no antiarrhythmic treatment was prescribed. The patients were followed up for a period of 20.6 +/- 11.2 months. The end points were occurrence of documented spontaneous sustained ventricular arrhythmia and sudden death. None of the 19 non-inducible patients experienced sudden death or spontaneous sustained ventricular arrhythmia. Two of the nine inducible patients died suddenly (P = 0.1). The 3-year sudden death mortality rate of the whole group was 7.5%. We conclude that when cardiac patients with high grade ventricular ectopy and left ventricular systolic dysfunction are treated according to the results of electrophysiological studies, it can be expected that their 3-year mortality rate will be low and significantly inferior to that reported for conventionally treated patients.

Adult↗
PubMed2003

Reversible ventricular dysfunction (takotsubo cardiomyopathy) following polymorphic ventricular tachycardia.

A 67-year-old female with recurrent syncope and no obvious heart disease developed ventricular dysfunction, known as takotsubo cardiomyopathy, following a 90 s episode of polymorphic ventricular tachycardia originating from a ventricular extrasystole with a short coupling interval. Cardiac catheterization performed 30 min after the arrhythmic event revealed angiographically normal coronary arteries, and left ventricular apical akinesis and basal hyperkinesis. An intracoronary injection of acetylcholine revealed no inducible coronary spasm, and an electrophysiological study revealed normal atrioventricular conduction and no inducible ventricular arrhythmia. Thirty hours after the arrhythmic event, electrocardiography revealed deeply inverted T waves in leads V3 to V6, I, and aVL, which continued for more than a week. Although no treatment was given to maintain hemodynamic stability, echocardiography revealed normal left ventricular contraction 14 days after the onset of the ventricular dysfunction. The reversible ventricular dysfunction might have been induced by altered catecholamine dynamics due to the persistent syncope during the occurrence of tachycardia.

Aged↗
PubMed1988

Left ventricular dysfunction due to chronic right ventricular pressure overload. Resolution following percutaneous balloon valvuloplasty for pulmonic stenosis.

Left ventricular dysfunction due to chronic right ventricular pressure overload is well documented in experimental animals, but is controversial in humans. Whether left ventricular dysfunction resolves following the relief of chronic right ventricular pressure overload has not been studied. In this report, rapid improvement in both right and left ventricular function following successful percutaneous balloon valvuloplasty is described in a patient with severe isolated valvular pulmonic stenosis and biventricular dysfunction. It appears that: (1) geometric distortion played a major role in his reversible left ventricular dysfunction, and (2) severe biventricular dysfunction should not be a contraindication to valvuloplasty for valvular pulmonic stenosis.

Adult↗
PubMed1981

Right ventricular dysfunction in acute ventricular septal defect.

Eight patients with acute ventricular septal defect (VSD) receiving early intra-aortic balloon augmentation, cardiac catheterization, and open-heart surgery are described. Because of the large shunts in this group of patients, there was visualization of the right ventricle during left ventriculography which was adequate for qualitative analysis. The following were noted: (1) All patients had severe right ventricular (RV) dysfunction angiographically. (2) RV akinesis noted on angiography was more extensive than the surgical description of RV infarction, although all patients had biventricular infarction at surgery. (3) The RV dysfunction was the major cause of death (two cases) or a contributing factor (three cases). (4) RV papillary muscle rupture was identified in one case.

Acute Disease↗
PubMed1988

Conventional and right precordial ECGs, creatine kinase, and radionuclide angiography in post-traumatic ventricular dysfunction.

Right ventricular infarction due to ischemic heart disease can be diagnosed by a right precordial electrogram or by first-pass radionuclide angiography (FPRNA). Prior FPRNA studies have shown that cardiac dysfunction after blunt chest trauma (myocardial contusion) is most often due to right ventricular dysfunction. We hypothesized that right ventricular dysfunction due to ischemic heart disease and myocardial contusion should produce similar ECG changes due to myocyte disruption. The purpose of our study was to evaluate the diagnostic value of the right precordial electrogram in suspected cardiac contusion. Thirty-five patients with suspected myocardial contusion based on mechanism of injury/clinical findings and no history of clinical heart disease were enrolled prospectively. All patients had conventional ECG, right precordial electrogram, and FPRNA studies. Twenty patients had normal cardiac scans (group 1); percentage of myocardial creatine kinase (CK-MB) was measured in 12 of these patients and was less than 5% in 11. Fifteen patients had abnormal cardiac scans (wall motion abnormality and/or decreased right ventricular ejection fraction) (mean, 34% +/- 7% [SD]; normal, greater than 40%) (group 2); percentage of CK-MB was measured in 13 of 15 patients and was less than 5% in all 13. Conventional ECGs and right precordial electrograms in all patients were analyzed for differences in heart rate, PR interval, QRS duration, corrected QT interval, and the axis of the frontal and horizontal plane QRS complex and ST segment. There were no significant differences between group 1 and group 2 patients. No patient with myocardial contusion diagnosed by FPRNA had elevated ST segments in V4R through V6R or a percentage CK-MB of more than 5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Late survival after valve operation in patients with left ventricular dysfunction.

BACKGROUND: Left ventricular dysfunction is a predictor of hospital mortality after cardiac valve operation. We evaluated late survival in a large cohort of these patients. METHODS: From 1980 to 1993, 257 patients with a preoperative ejection fraction of 0.40 or less underwent aortic (n = 177), mitral (n = 72), or combined (n = 8) valve operation, with or without concomitant coronary artery bypass grafting. RESULTS: Hospital mortality was 12.5%. Follow-up was 98% complete. Logistic regression analysis showed that an ejection fraction of less than 0.30, mitral regurgitation, concomitant coronary artery bypass grafting, emergency operation, and reoperation were independent correlates of hospital mortality (all at p < 0.05). Kaplan-Meier survival curves of the 220 hospital survivors showed a 65% 5-year survival. Multivariate analysis revealed preoperative use of diuretics, male sex, reoperation, age exceeding 60 years, and aortic regurgitation to be independent predictors of poor late outcome (all at p < 0.05). CONCLUSIONS: The liability of left ventricular dysfunction with regard to diminished long-term survival is not completely reversed by valve operation. If operation is not performed before left ventricular dysfunction develops, postoperative medical treatment of these dilated, remodeled ventricles should be considered.

Adolescent↗
PubMed2004

Selective microembolization of the circumflex coronary artery in an ovine model: Dilated, ischemic cardiomyopathy and left ventricular dysfunction.

BACKGROUND: Ventricular remodeling often occurs after myocardial infarction, yet the natural history remains unpredictable because of the chronicity of the process and therapeutic interventions involved. We induced cardiac dysfunction in an ovine model via selective microembolization of the circumflex coronary artery (LCx) to test the hypothesis that ventricular remodeling progresses following coronary microembolization for up to 24 months. Methods and results Sheep underwent weekly selective microembolization of the LCx until left ventricular ejection fraction stabilized <35% for 2 consecutive weeks. In a subgroup carried out to 4 months, the end-systolic pressure-volume relationship slope decreased from 2.3+/-0.6 (baseline) to 1.3+/-0.5 at month 4 (P<.05). In a second group, echocardiography at 24 months, the ejection fraction decreased from 51+/-3% (baseline) to 25+/-2% (month 5) (P<.05) and stabilized through month 24 (23+/-5%, P<.05), whereas left ventricular end-systolic area and left ventricular end-diastolic area increased by 222% and 98%, respectively, through month 24. CONCLUSIONS: Selective microembolization of the LCx induces left ventricular dysfunction followed by dilated, ischemic cardiomyopathy, which continues to progress for up to 2 years despite stabilization of left ventricular ejection fraction. This model of ventricular remodeling secondary to microinfarction may be a useful experimental platform for large animal heart failure investigations.

Animals↗
PubMed2002

Nitric oxide production is maintained in exercising swine with chronic left ventricular dysfunction.

Left ventricular (LV) dysfunction caused by myocardial infarction (MI) is accompanied by endothelial dysfunction, most notably a loss of nitric oxide (NO) availability. We tested the hypothesis that endothelial dysfunction contributes to impaired tissue perfusion during increased metabolic demands as produced by exercise, and we determined the contribution of NO to regulation of regional systemic, pulmonary, and coronary vasomotor tone in exercising swine with LV dysfunction produced by a 2- to 3-wk-old MI. LV dysfunction resulted in blunted systemic and coronary vasodilator responses to ATP, whereas the responses to nitroprusside were maintained. Exercise resulted in blunted systemic and pulmonary vasodilator responses in MI that resembled the vasodilator responses in normal (N) swine following blockade of NO synthase with N(omega)-nitro-L-arginine (L-NNA, 20 mg/kg iv). However, L-NNA resulted in similar decreases in systemic (43 +/- 3% in N swine and 49 +/- 4% in MI swine), pulmonary (45 +/- 5% in N swine and 49 +/- 4% in MI swine), and coronary (28 +/- 4% in N and 35 +/- 3% in MI) vascular conductances in N and MI swine under resting conditions; similar effects were observed during treadmill exercise. Selective inhibition of inducible NO synthase with aminoguanidine (20 mg/kg iv) had no effect on vascular tone in MI. These findings indicate that while agonist-induced vasodilation is already blunted early after myocardial infarction, the contribution of endothelial NO synthase-derived NO to regulation of vascular tone under basal conditions and during exercise is maintained.

Adenosine Triphosphate↗
PubMed2006

Paradoxical contributions of non-compacted and compacted segments to global left ventricular dysfunction in isolated left ventricular noncompaction.

The pathophysiologic mechanisms of left ventricular (LV) dysfunction in isolated ventricular noncompaction (IVNC) remain unclear. Evaluating global and segmental systolic LV function in 65 patients with IVNC, this study found that normal wall motion was more common in noncompacted than in compacted segments. The number of noncompacted segments per patient correlated positively with the LV ejection fraction and negatively with LV end-diastolic volume index. These paradoxical findings support the concept that noncompaction represents a marker of a more generalized (cardio)myopathy rather than the direct pathophysiologic substrate of this still little-understood disease.

Adult↗
PubMed1996

Angina and left ventricular dysfunction.

Angina with left ventricular dysfunction exhibits a wide range of different presentations. Approximately 45% of patients referred for coronary artery bypass surgery have some degree of left ventricular dysfunction and, given that at least a third of those suffering from angina have a history of myocardial infarction, the prevalence of left ventricular dysfunction in such patients is likely to be substantial. The major prognostic factor in patients with coronary artery disease is the degree of left ventricular function and it is important to identify those with poor or reduced left ventricular function. High-risk patients, defined by exercise testing and echocardiography, should be considered for revascularization. For the majority of patients management should be medical, consisting of nitrates plus a beta-blocker or calcium antagonist. In severe ischaemia, the combination of these agents has been shown to provide additional efficacy. In patients with heart failure the newer calcium antagonist amlodipine has been shown to have a neutral effect upon survival, indicating that it may be used safely in patients with angina and left ventricular dysfunction. Progression of left ventricular dysfunction may be slowed through the use of angiotensin converting enzyme (ACE) inhibitors, which have also been shown to improve survival, although they should be used with caution, since there is evidence that ACE inhibitors may worsen angina in some patients.

Angina Pectoris↗
PubMed2006

[Takotsubo-like left ventricular dysfunction with delayed recovery of left ventricular shape: a case report].

A 70-year-old woman was admitted to our hospital because of left ventricular dysfunction, which was observed after permanent pacemaker implantation in another hospital. The left ventricular dysfunction was apical ballooning. Left ventriculography demonstrated takotsubo-like shape. However, the dysfunction did not improve immediately with medical treatment. In this case, 75% stenosis was observed in the left anterior descending artery. We suppose that this lesion corresponded to the delayed recovery of the dysfunction and performed coronary intervention. The takotsubo-like shape improved gradually for about 1 year. Whether the coronary intervention was effective for the recovery of the dysfunction is unclear, this clinical course was interesting in evaluating the delayed recovery of takotsubo-like left ventricular dysfunction.

Aged↗
PubMed1987

Stress induced right ventricular dysfunction: an indication of reversible right ventricular ischaemia.

Stress induced changes in left ventricular ejection fraction are widely used in the detection and assessment of coronary artery disease. This study demonstrates that right ventricular dysfunction may also occur, and assesses its significance in terms of coronary artery anatomy. This study involved 14 normal subjects and 26 with coronary artery disease investigated by equilibrium radionuclide ventriculography, at rest and during maximal dynamic exercise. Mean normal resting right ventricular ejection fraction (RVEF) was 0.40 (SD 0.118), and all normal subjects increased RVEF with stress (mean delta RVEF + 0.13 SD 0.099). Mean delta RVEF in the subjects with coronary artery disease was significantly lower at 0.00 (SD 0.080), but there was overlap between the two groups. The largest falls in RVEF were seen if the right coronary artery was occluded without retrograde filling. In this subgroup with the most severely compromised right ventricular perfusion (nine subjects), RVEF always fell with stress, and mean delta RVEF was -0.08 (SD 0.050). There was no significant correlation between delta LVEF and delta RVEF, implying that the right ventricular dysfunction was due to right ventricular ischaemia, rather than secondary to left ventricular dysfunction. Stress induced right ventricular ischaemia can therefore be detected readily by radionuclide ventriculography.

Adult↗
PubMedDate not supplied

Spontaneous resolution of severe right ventricular dysfunction in right ventricular infarction: documentation by radionuclide studies.

A case of inferior myocardial infarction complicated by severe arrhythmias and right heart failure is presented. Radionuclide studies performed near the acute phase and one month later illustrate the reversibility of right heart dysfunction caused by infarction. Signs of right ventricular involvement in acute inferior myocardial infarction are noted in about 40% of cardiac blood-pool studies: right ventricular dilatation with a significantly decreased ejection fraction, and ventricular wall motion abnormalities. Follow-up studies in the recovery period show good recovery of right ventricular function.

Aged↗
PubMed1992

Comparison of painful and painless left ventricular dysfunction recorded during ambulatory ventricular function monitoring in angina pectoris secondary to coronary artery disease.

Left ventricular (LV) function and the electrocardiogram of 55 patients with coronary artery disease and angina were monitored for a mean of 3.2 +/- 1.9 hours with an ambulatory LV function monitor. During the monitoring interval, patients performed daily activities such as sitting, walking, climbing stairs, and eating. Sixty episodes of transient reduction in ejection fraction of > 5% lasting > 60 seconds were observed in 24 patients; 13 episodes were associated with typical angina, but 47 were asymptomatic. Asymptomatic episodes had a shorter duration of ventricular dysfunction (116 +/- 49 vs 189 +/- 113 seconds; p < 0.05), and smaller increases in relative end-diastolic and end-systolic volumes (end-diastolic 0.9 +/- 5.4% vs 4.6 +/- 4.9% [p < 0.05], and end-systolic 21 +/- 11% vs 35 +/- 20% [p < 0.05]) than did symptomatic ones. When a subset of patients with both symptomatic and asymptomatic episodes were analyzed, similar results were observed: in asymptomatic episodes, duration was shorter (82 +/- 31 vs 200 +/- 110 seconds; p < 0.005), ejection fraction decrease was smaller (-7.3 +/- 2.6% vs -11.0 +/- 4.7%; p < 0.05), and end-systolic volume increase was smaller (23 +/- 12% vs 37 +/- 19%; p < 0.05). The data suggest that asymptomatic transient LV dysfunction is less severe and of shorter duration in patients with angina pectoris.

Angina Pectoris↗
PubMed2000

Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

OBJECTIVE: Rapid ventricular pacing produces a reliable model of heart failure. Cessation after 4 weeks of rapid ventricular pacing results in rapid normalization of left ventricular function, but the left ventricle remains persistently dilated. We present novel data that show that prolonged rapid ventricular pacing (10 weeks) creates a model of chronic left ventricular dysfunction. METHODS: In 9 dogs undergoing 10 weeks of rapid ventricular pacing, left ventricular function and volumes were serially assessed by using 2-dimensional echocardiography and pressure-volume analysis for 12 weeks after cessation of pacing. RESULTS: Increased end-diastolic volume and decreased systolic and diastolic function were seen at the end of pacing. By 2 weeks of recovery from rapid ventricular pacing, end-diastolic volume and ejection fraction were partially recovered but did not improve further thereafter. Load-independent and load-sensitive indices of function obtained by pressure-volume analysis at 8 and 12 weeks of recovery confirmed a persistence of both systolic and diastolic dysfunction. In addition, left ventricular mass increased with pacing and remained elevated at 8 and 12 weeks of recovery. Four of these dogs studied at 6 months of recovery showed similar left ventricular abnormalities. CONCLUSION: Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

Animals↗
PubMed1980

Ventricular compliance in ischemic right ventricular dysfunction.

Ischemic right ventricular dysfunction was diagnosed in 54 patients with acute myocardial infarction who had a right atrial pressure disproportionately increased in relation to the pulmonary capillary pressure. The right atrial pressure curve in 40 patients (74 percent) was M- or W-shaped, termed a noncompliant pattern, and was similar to the pattern found in constrictive pericarditis. Kussmaul's sign was found in the patients whose respiration was recorded. This pattern, which represents poor right ventricular compliance, was severe in 30 cases (y descent greater than x descent) and slight in 10 cases (y descent = x descent). Its duration was variable, ranging from days to years. Of the 54 patients, 32 (59 percent) had a low output syndrome, diagnosed in the presence of a cardiac index of less than 2.2 liters/min per m2, with signs of poor tissue perfusion. The severe noncompliant pattern was significantly related to the presence of a low output syndrome (p less than 0.01) and mortality from this cause (p less than 0.05). The jugular venous tracing pulse had a pattern similar to that of the right atrial pressure recording and therefore may be valuable in the noninvasive diagnosis of right ventricular dysfunction and in the study of the evolution of the noncompliant pattern and, hence, of ventricular compliance.

Acute Disease↗