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PubMed1986

Effect of beta-blockade on right ventricular performance in patients with and without right ventricular dysfunction due to coronary artery disease.

To assess the effects of beta-blockade on right ventricular performance in patients with and without right ventricular dysfunction due to coronary artery disease, we performed radionuclide ventriculography on eight patients with normal right ventricular ejection fraction (RVEF greater than or equal to 35%) and 14 patients with mild to moderate right ventricular dysfunction (RVEF less than 35%) at rest. All patients had chronic stable angina pectoris, and nine patients had prior myocardial infarction. Radionuclide ventriculography was performed on placebo and during clinical beta-blockade (heart rate, 50 to 60 beats per minute and less than or equal to 20% increase in heart rate over baseline during stage I treadmill exercise, Bruce protocol) with the oral, cardioselective beta-blocking agent, betaxolol. The resting RVEF (mean +/- 1 SD) was 33% +/- 7% on placebo and 34% +/- 7% during clinical beta-blockade. Mean exercise RVEF was 40% +/- 8% on placebo and 39% +/- 8% during clinical beta-blockade. These differences were not statistically significant. Resting left ventricular ejection fraction ranged from 22% to 60% (mean, 42% +/- 8%). On placebo, one of eight patients with a resting RVEF greater than or equal to 35% had a normal exercise RVEF response (greater than or equal to 5% increment) whereas nine of 14 patients with resting RVEF less than 35% had normal exercise response. The discordant relationship between baseline RVEF and exercise response on placebo became less marked during clinical beta-blockade. We conclude that beta-blockade does not produce significant deterioration of right ventricular systolic function or right ventricular reserve either in patients with normal or in those with mild to moderately impaired resting right ventricular systolic function.

Adrenergic beta-Antagonists↗
PubMed1997

Nitric oxide inhalation in the treatment of right ventricular dysfunction following left ventricular assist device implantation.

BACKGROUND: Following left ventricular assist device (LVAD) implantation in end-stage heart failure, the management of right ventricular dysfunction presents a therapeutic problem unresolved by conventional drug therapy (catecholamines, nitrates, and prostacyclin). This study was performed to investigate the effects of supplemental inhalation of nitric oxide (NO), a selective pulmonary vasodilator, postoperatively and prospectively. METHODS AND RESULTS: Intraindividual dose titration of NO was performed (0 to 40 ppm) according to a standardized protocol. Thereafter treatment was continued with the individually most effective dose of NO (25 to 40 ppm). In 8 consecutive male patients presenting with right ventricular dysfunction postoperatively, a significant dose-dependent improvement in hemodynamic function was observed: pulmonary vascular resistance decreased from 336+/-110 to 210+/-59 dynes x s x cm(-5) (P<.0001), cardiac index rose from 2.0+/-0.4 to 2.7+/-0.4 L x min(-1) x m(-2) (P<.003) at 40 ppm; doses of >20 ppm were effective in increasing cardiac index (P<.05). With continuous NO inhalation up to 48 hours, pulmonary vascular resistance decreased further to 155+/-33 dynes x s x cm(-5) (P<.0001) as the cardiac index increased to 3.3+/-0.6 L x min(-1) x m(-2) (P<.003). Pulmonary artery pressure decreased (P<.0001) as did systemic vascular resistance with hemodynamic improvement (P<.01). Central venous pressure and mean arterial pressure remained unchanged. Right ventricular ejection fraction at transesophageal echocardiography increased from 24+/-7% to 44+/-7% (P<.01) at the end of the study, and right ventricular end-diastolic volume decreased (P<.05). Weaning from NO therapy was successful at 2 to 8 days, and all patients were extubated. Right ventricular function remained stable thereafter. CONCLUSIONS: In the treatment of right ventricular dysfunction following LVAD implantation, inhalation of NO markedly decreased right ventricular afterload by its selective vasodilating effects on the pulmonary circulation without producing systemic hypotension; this merits further evaluation.

Administration, Inhalation↗
PubMedDate not supplied

[Ventricular tachycardia associated with isolated right ventricular dysfunction as indicator of arrhythmogenic dysplasia of the right ventricle].

We report the case of a 21 year-old patient with arrhythmogenic right ventricular dysplasia manifested by episodes of QRS tachycardia greater than 0.12 sec and isolated dysfunction of the right ventricle. The patient treated with amiodarone however, the tachycardia episodes persisted. The surface electrocardiogram showed left branch block with the axis down, which suggested a right ventricle origin, and was therefore considered an arrhythmogenic dysplasia. Echocardiography and cardioangiography showed alterations in the anatomy of the outflow tract of the right ventricle. A myocardial gammagraphy revealed no perfusion alterations. The endomyocardial biopsy showed perivascular fibrosis. An electrophysiology study was performed, stimulating the outflow tract of the right ventricle, which induced two types of ventricular tachycardias, one of them identical to that recorded clinical. The patient was treated with sotalol, and has been being free of ventricular tachycardia episodes for 18 months of follow-up. We consider that this entity should be studied in a systematic way in those patients with ventricular tachycardia originated in the outflow of the right ventricle and with primary cardiac illness.

Adult↗
PubMed2004

[Right ventricular dysfunction and ischemia in pulmonary embolism].

Patients with pulmonary embolism and right ventricle dysfunction (determined with clinical, hemodynamic or echocardiographic methods) are a subgroup at high risk for complications. One of the pathogenic factors of right ventricular dysfunction in pulmonary embolism is myocardial ischemia, usually secondary to hemodynamic overload, and sometimes worsened by underlying coronary artery disease. We described a patient with pulmonary embolism and dyskinesia of the right ventricular free wall, related to chronic atherosclerotic occlusion of the right coronary artery proximal to the acute marginal branches that irrigate the free wall.

Aged↗
PubMed1997

Right ventricular dysfunction in patients with obstructive sleep apnoea syndrome.

There is conclusive evidence that obstructive sleep apnoea syndrome (OSAS) influences right heart haemodynamics and can also induce pulmonary hypertension. It is not known, however, whether right ventricular dysfunction can occur in patients with OSAS in the absence of lung disease. We studied 107 patients (94 males, 13 females, mean age 55 +/- 11 yrs) with polysomnographically verified OSAS in whom clinically significant lung disease was excluded. Right ventricular ejection fraction (RVEF) was determined by radionuclide ventriculography. In addition, pulmonary function tests, arterial blood gas analysis and right heart catheterization were performed. RVEF was impaired in 19 patients (18%). Eighteen (95%) had signs or symptoms consistent with mild right ventricular failure. Patients with or without impaired RVEF did not differ with respect to body mass index, age or lung function. Stepwise multiple logistic regression analysis revealed that RVEF was significantly associated with the apnoea/hypopnoea index (r = -0.68; p = 0.0009) and the extent of nocturnal oxyhaemoglobin saturation (r = 0.42; p = 0.035), but not with age, body mass index, blood gas analysis, gender, lung function, pulmonary artery pressure and left ventricular ejection fraction. We conclude that in patients with otherwise unexplained right ventricular failure, obstructive sleep apnoea syndrome may underlie the right ventricular dysfunction.

Adult↗
PubMed2006

Association of persistent right ventricular dysfunction at hospital discharge after acute pulmonary embolism with recurrent thromboembolic events.

BACKGROUND: In patients with acute pulmonary embolism, right ventricular dysfunction (RVD) on hospital admission is a predictor of adverse short-term clinical outcome. The aim of this study was to evaluate the prognostic value of RVD persistence at hospital discharge with regard to the likelihood of recurrent venous thromboembolism (VTE). METHODS: Echocardiography was used to assess RVD on admission and before hospital discharge in 301 consecutive patients with the first episode of acute pulmonary embolism occurring from January 1998 through July 2004. Right ventricular dysfunction was diagnosed in the presence of 1 or more of the following: right ventricular dilation (without hypertrophy), paradoxical septal systolic motion, and Doppler evidence of pulmonary hypertension. Patients were followed up at 2, 6, and 12 months and yearly thereafter. The primary end point was symptomatic, recurrent fatal or nonfatal VTE. RESULTS: Patients were categorized as those (1) without RVD (155 patients [51.5%]), (2) with RVD regression (RVD on admission but not at discharge; 87 patients [28.9%]), and (3) with persistent RVD (RVD on admission and at discharge; 59 patients [19.6%]). After a mean +/- SD of 3.1 +/- 2.7 years, patients with RVD persistence showed an increased risk of recurrent VTE (14 patients, 9.2% patient-years) compared with those without RVD (15 patients, 3.1% patient-years) or RVD regression (3 patients, 1.1% patient-years) (P = .001). Six of 8 deaths related to pulmonary embolism occurred in patients with RVD persistence. At multivariate analysis, adjusted by anticoagulant treatment duration, RVD persistence was an independent predictor of recurrent VTE (hazard ratio, 3.79; P<.001). CONCLUSION: Persistent RVD at hospital discharge after an acute pulmonary embolism is associated with recurrent VTE.

Acute Disease↗
PubMed2004

Regional and global right ventricular dysfunction in asymptomatic or minimally symptomatic patients with congenitally corrected transposition.

Patients with congenitally corrected transposition are at risk of right ventricular dysfunction and failure. With this in mind, we examined 13 patients with congenitally corrected transposition, 7 not having undergone surgery, and 6 after physiological repair, comparing them with 6 healthy subjects matched for age and sex, using cardiac magnetic resonance imaging, at rest and during dobutamine stress, in order to determine regional and global right ventricular response to stress. At rest, the patients had significantly decreased overall wall motion compared to their healthy peers (7.2 +/- 0.5, versus 9.8 +/- 0.4 mm). During infusion of dobutamine, overall wall motion increased to 12.8 +/- 0.4 mm in the healthy subjects, versus 8.8 +/- 1.0 mm in patients. At the regional level, significant differences in mural motion were found between patients and controls in the anterior (9.5 +/- 1.1, versus 13.2 +/- 0.6 mm), posterior (10.2 +/- 1.6, versus 13.2 +/- 0.8 mm), and septal segments (5.0 +/- 0.8, versus 11.2 +/- 0.6 mm). At rest, overall mural thickening in patients was similar to that of controls, but significantly less in patients during stress. During dobutamine stress, patients showed significantly less regional wall thickening than controls, particularly in the septal (2.7 +/- 0.6, versus 6.0 +/- 0.4 mm, respectively) and in the anterior segments (4.2 +/- 0.6, versus 7.8 +/- 0.6 mm, respectively). Right ventricular ejection fraction strongly correlated with mural motion and thickening, both at rest and during stress. Abnormal regional function in the systemic morphologically right ventricle may occur in patients with congenitally corrected transposition, which strongly correlates with right ventricular ejection fraction. Our findings support the hypothesis that, in patients with congenitally corrected transposition, ischemia of the right ventricular myocardium contributes to the development of right ventricular dysfunction.

Adult↗
PubMed2006

Inhaled iloprost in eight heart transplant recipients presenting with post-bypass acute right ventricular dysfunction.

BACKGROUND: During heart transplantation, weaning from cardiopulmonary bypass may be particularly laborious as a result of superimposed acute right ventricular dysfunction in the setting of pre-existing pulmonary hypertension. Research in recent years has focused on inhaled vasodilatory treatment modalities which selectively target the pulmonary circulation. METHODS: We present a series of eight patients in whom inhaled iloprost, a synthetic prostacyclin analog, was used to treat pulmonary hypertension and right ventricular dysfunction detected by transesophageal echocardiography during a heart transplant procedure. In addition to conventional inotropic support, 20 mug of inhaled iloprost was administered via nebulized aerosol for a 20-min period. Complete sets of hemodynamic measurements were obtained before inhalation and during and after cessation of the inhalation period. RESULTS: Inhaled iloprost decreased the transpulmonary gradient at the end of the inhalation period relative to baseline (8.2 +/- 1.6 mmHg vs. 11.2 +/- 0.9 mmHg, P < 0.05). The mean pulmonary artery pressure to systemic artery pressure ratio decreased over this period (0.24 +/- 0.07 vs. 0.44 +/- 0.09, P < 0.05). A statistically significant decrease in the pulmonary vascular resistance to systemic vascular resistance ratio was also observed (0.10 +/- 0.02 vs. 0.19 +/- 0.02, P < 0.05). Improved indices of right ventricular function were observed in echocardiographic monitoring. CONCLUSION: During heart transplantation procedures, episodes of pulmonary hypertension can be successfully treated with inhaled iloprost administration, without untoward side-effects or significant systemic impact.

Administration, Inhalation↗
PubMed2006

Cardiac inflammation contributes to right ventricular dysfunction following experimental pulmonary embolism in rats.

Acute right ventricular (RV) failure following pulmonary embolism (PE) is a strong predictor of poor clinical outcome. Present studies test for an association between RV failure from experimental PE, inflammation, and upregulated chemokine expression. Additional experiments test if neutrophil influx contributes to RV dysfunction. PE was induced in male rats by infusing 24 microm microspheres (right jugular vein) producing mild hypertension (1.3 million beads/100 g, PE1.3), or moderately severe hypertension (2.0 million beads/100 g, PE2.0). Additional rats served as vehicle sham (0.01% Tween 20, Veh). In vivo RV peak systolic pressures (RVPSP) increased significantly, and then declined following PE2.0 (51 +/- 1 mm Hg 2 h; 49 +/- 1, 6 h; 44 +/- 1, 18 h). RV generated pressure of isolated, perfused hearts was significantly reduced in PE2.0 compared with PE1.3 or Veh. MCP-1 protein (ELISA) was elevated 21-fold and myeloperoxidase activity 95-fold in RV of PE2.0 compared with Veh or PE1.3. CINC-1, CINC-2, MIP-2, MCP-1, and MIP-1alpha mRNA also increased in RV of PE2.0. Histological analysis revealed massive accumulation of neutrophils (selective esterase stain) and monocyte/macrophages (CD68, ED-1) in RV of PE2.0 hearts in regions of myocyte damage. Electron microscopy showed myocyte necrosis and phagocytosis by inflammatory cells. LV function was normal and did not show increased inflammation after PE2.0. Treatment with anti-PMN antibody reduced RV MPO activity and prevented RV dysfunction. Conclusions-PE with moderately severe pulmonary hypertension (PE2.0) resulted in selective RV dysfunction, which was associated with increased chemokine expression, and infiltration of both neutrophils and monocyte/macrophages, indicating that a robust immune response occurred with RV damage following experimental PE. Experimental agranulocytosis reduced RV, suggesting that neutrophil influx contributed to RV damage.

Animals↗
PubMed2005

Pulmonary hypertension and right ventricular dysfunction in growth-restricted, extremely low birth weight neonates.

This case series reports an acute episode of hypoxemia and systemic hypotension in seven infants under 1 kg, taking place several hours or days after birth, after a period of stability and in the absence of significant lung disease. These patients were growth-restricted at birth and had a history of chronic fetal hypoxia and oligohydramnios. Pulmonary hypertension and right ventricular dysfunction were found by echocadiography. Right ventricular ejection fraction was significantly depressed during the acute episode, compared to baseline values measured after recovery. The timing of symptoms seemed related to ductus arteriosus closure or constriction. Oxygenation and right ventricular function improvement occurred within a few days under ventilatory and inotropic support, while milrinone was administered in five cases. In conclusion, pulmonary hypertension is a rare but significant cause of hypoxemia in preterm infants, and pulmonary vasodilator therapy should be considered in the presence of right ventricular dysfunction.

Acute Disease↗
PubMed2000

Left ventricular reconditioning and anatomical correction for systemic right ventricular dysfunction.

The morphologically right ventricle (mRV) fails after managing systemic workload for a variable period of time in some patients with transposition of the great arteries (TGA) who have undergone an atrial switch operation and in patients with congenitally corrected transposition of the great arteries (cc-TGA). Conventional therapy for progressive mRV failure, including tricuspid valve replacement and cardiac transplantation, has been disappointing. Anatomical correction, reincorporating the morphologically left ventricle (mLV) into systemic circulation, was performed in a total of 84 patients (39 TGA, 45 cc-TGA) in 2 institutions (Royal Children Hospital 1981-1993; Cleveland Clinic Foundation 1993-1999). The mVL was retrained to generate systemic pressure by means of pulmonary artery band in 43 patients. The overall mortality for patients entering this program is 15.4% (8 early and 5 late operative deaths). All of the operative deaths were patients with TGA and a prior atrial switch operation. Four patients (5%) have been transplanted or are on a transplantation waiting list. In patients with TGA and previous atrial switch operation, older age and abnormal coronary anatomy was associated with a higher operative mortality. None of the measured parameters of the mLV and mRV were predictors of failure of mLV reconditioning. Follow-up echocardiographic evaluations of the 46 survivors of anatomical correction showed normal mRV function in 41 (89%) and normal mLV function in 42 patients (91%). mLV retraining and anatomical correction produces good results in prepubescent patients. The response of older patients is less predictable and associated with a higher early and late mortality. Copyright 2000 by W.B. Saunders Company

Journal Article↗
PubMed1990

Serial evaluation of right ventricular dysfunction associated with acute inferior myocardial infarction.

Right ventricular (RV) function was evaluated serially by multigated blood pool imaging in 18 patients with RV dysfunction associated with acute inferior myocardial infarction. Radionuclide ventriculograms were performed on all patients within 18 hours of chest pain and again at 10 days. In addition, 15 of 18 patients had rest and exercise radionuclide ventriculograms at 3 months. The mean resting right ventricular ejection fractions (RVEF) at admission, 10 days, and 3 months in these patients was 31.8 +/- 12.6% (SD), 46.9 +/- 11.2% (p less than 0.05), and 44.5 +/- 10.2% (p less than 0.05), while the left ventricular ejection fractions were 55.9 +/- 10.6%, 57.9 +/- 13.3%, and 53.1 +/- 11.2% (p = ns). The 3-month exercise radionuclide ventriculogram demonstrated an increase in RVEF greater than 5% in 6 of 15 patients. In eight catheterized patients, neither the location nor the severity of coronary artery narrowing nor the presence of collaterals correlated with the RV exercise response. Improvement in RV function over a 10-day interval following acute inferior myocardial infarction suggests the presence of significant reversible right ventricular dysfunction during the acute phase.

Cardiac Catheterization↗
PubMed2006

Association of subclinical right ventricular dysfunction with obesity.

OBJECTIVES: The purpose of this research was to identify the determinants of right ventricular (RV) dysfunction in overweight and obese subjects. BACKGROUND: Right ventricular dysfunction in obese subjects is usually ascribed to comorbid diseases, especially obstructive sleep apnea. We used tissue Doppler imaging to identify the determinants of RV dysfunction in overweight and obese subjects. METHODS: Standard and tissue Doppler echocardiography was performed in 112 overweight (body mass index [BMI] 25 to 29.9 kg/m2) or obese (BMI >30 kg/m2) subjects and 36 referents (BMI <25 kg/m2), including 22 with obstructive sleep apnea but no obesity. Tissue Doppler was used to measure RV systolic (s(m)) and diastolic (e(m)) velocities and strain indexes. RESULTS: Obese subjects with BMI >35 kg/m2 had reduced RV function compared with referent subjects, evidenced by reduced s(m) (6.5 +/- 2.4 cm/s vs. 10.2 +/- 1.5 cm/s, p < 0.001), peak strain (-21 +/- 4% vs. -28 +/- 4%, p < 0.001), peak strain rate (-1.4 +/- 0.4 s(-1) vs. -2.0 +/- 0.5 s(-1), p < 0.001), and e(m) (-6.8 +/- 2.4 cm/s vs. -10.3 +/- 2.5 cm/s, p < 0.001), irrespective of the presence of sleep apnea. Similar but lesser degrees of reduced systolic function (p < 0.05) were present in overweight (BMI 25 to 29.9 kg/m2) and mildly obese (BMI 30 to 35 kg/m2) groups. Differences in RV e(m), s(m), and strain indexes were demonstrated between the severely versus overweight and mildly obese groups (p < 0.05). Body mass index remained independently related to RV changes after adjusting for age, log insulin, and mean arterial pressures. In obese patients, these changes were associated with reduced exercise capacity but not the duration of obesity and presence of sleep apnea or its severity. CONCLUSIONS: Increasing BMI is associated with increasing severity of RV dysfunction in overweight and obese subjects without overt heart disease, independent of sleep apnea.

Adult↗
PubMed1987

[Mid-term outcome of acute right ventricular dysfunction in biventricular myocardial infarction. Hemodynamic and cineangiographic studies].

This study was designed to evaluate the mid-term outcome of the right ventricular (RV) dysfunction which characterizes infarction of both ventricles in the acute phase. Thirteen patients hospitalized for inaugural posterior or infero-posterior infarction extending to the right ventricle (haemodynamic and cineangiographic diagnosis) were explored in the acute phase and 4 months later by right heart catheterization and selective cineangiography of the right ventricle in a 30 degrees RAO projection. The results were compared with those obtained in a control group. Haemodynamically, the RV filling pressures (p less than 0.001) and the indices of RV dysfunction--i.e. RV end-diastolic pressure/RV systolic pressure ratio (p less than 0.001) and right atrial pressure/pulmonary wedge pressure ratio (p less than 0.02)--were significantly decreased between the acute and chronic phases, but they remained pathological compared with those measured in the control group. Angiographically, the right ventricular dysfunction in the acute phase was reflected in an increase of the RV end-systolic volume (p less than 0.02) and a decrease of the RV ejection fraction (p less than 0.01), whereas diastolic cavitary dilatation was inconstant, with mean values of RV end-diastolic volume close to those found in the control group. The systolic dysfunction persisted, unchanged, during the chronic phase. Segmental kinetics of the inferior wall was much reduced in the acute phase (p less than 0.001), this hypokinesia partially regressing in the chronic phase; but in fact there were wide individual variations, and some patients even recovered an almost normal contractility. Tricuspid valve regurgitation was frequent (6/13 cases) in the acute phase and regressed in 2 out of 3 cases in the chronic phase; its presence introduced a degree of bias in the measurement of RV end-systolic volume and RV ejection fraction, with a tendency to underestimate the severity of diastolic dysfunction. To summarize, right ventricular dysfunction was constant but often modest in the acute phase and remained relatively stable at mid-term, whereas segmental kinetics of the inferior wall improved, sometimes dramatically.

Adult↗
PubMed2004

Long-term results of left ventricular reconditioning and anatomic correction for systemic right ventricular dysfunction after atrial switch procedures.

OBJECTIVES: Systemic right ventricular failure after atrial switch procedures for transposition of the great arteries has been addressed at Melbourne's Royal Children's Hospital (1981-1993) and the Cleveland Clinic Foundation (1993-2001) with reconditioning of the morphologically left ventricle by means of pulmonary artery banding followed by an arterial switch operation and an atrial reseptation. METHODS: Thirty-nine patients (Royal Children's Hospital, 19; Cleveland Clinic Foundation, 20) with a median age of 10.8 years (range, 13 months-24 years) entered this protocol a median of 10.3 years (range, 0.5-24 years) after an atrial switch procedure. RESULTS: The median duration of pulmonary artery banding was 13 months (range, 0.5-5.4 years). Ten (28%) patients responded unfavorably to morphologically left ventricular reconditioning (5 mortalities: 4 transplantations and 1 PAB still in place). Twenty-four (83%) of the 29 patients who underwent an atrial switch operation and atrial reseptation survived. During a median follow-up period of 8.2 years (range, 1-16 years), 3 patients had cardiac-related deaths. All 18 long-term survivors are asymptomatic. At last echocardiographic evaluation, the morphologically left ventricular function was normal or mildly decreased in 16 (89%) patients, and all had normal or mildly decreased systemic right ventricular function with no or mild tricuspid regurgitation. Age greater than 12 years was associated with a greater probability of morphologically left ventricular failure and not completing the protocol (P =.02) and a higher operative mortality at anatomic correction (P =.02). CONCLUSIONS: Morphologically left ventricular reconditioning and an anatomic correction protocol should be integrated into a cardiac transplantation program when treating patients with morphologically right ventricular failure after Mustard and Senning procedures. It is an alternative to cardiac transplantation in selected patients, with good long-term results. The response to morphologically left ventricular reconditioning past adolescence is inconsistent.

Adolescent↗
PubMed1994

Right ventricular dysfunction: an independent predictor of adverse outcome in patients with myocarditis.

To assess the predictive value of right ventricular systolic function in patients with active myocarditis, the echocardiograms of 23 patients with biopsy-confirmed myocarditis were reviewed. Right ventricular systolic function was evaluated qualitatively and quantitatively by descent of the right ventricular base. Patients were divided into those with normal right ventricular function, in whom right ventricular descent was 1.9 +/- 0.1 cm, and those with abnormal right ventricular function, in whom right ventricular descent was 0.8 +/- 0.1 cm (p < 0.001). There were no differences between the two groups in age, duration of symptoms, baseline hemodynamics, or histologic assessment. Initial left ventricular ejection fraction was significantly lower in patients with depressed right ventricular function (27.5 +/- 4.9%) compared with that in patients with normal right ventricular function (47.5 +/- 6.3%) (p = 0.01). The likelihood of an adverse outcome, defined as death or need for cardiac transplantation, was greater in patients with abnormal right ventricular function (right ventricular descent < or = 1.7 cm) than in patients with normal right ventricular function (right ventricular descent > 1.7 cm) (p < 0.03). Multivariate analysis revealed that right ventricular dysfunction as quantified by right ventricular descent was the most powerful predictor of adverse outcome.

Female↗
PubMed1997

Identification of severe right ventricular dysfunction by technetium-99m-sestamibi gated SPECT imaging.

An 84-yr-old man with previous anterior wall myocardial infarction presented with shortness of breath and palpitations. His symptoms were attributed to myocardial ischemia, and he was referred for a stress 99mTc-sestamibi SPECT imaging study with gating. The images showed minimal left ventricular ischemia, but a dilated and hypokinetic right ventricle suggested pulmonary pathology as the probable etiology of his presenting symptoms. A subsequent ventilation perfusion study was consistent with the diagnosis of multiple pulmonary emboli. Thus, 99mTc-sestamibi SPECT imaging with gating provides information about right ventricular perfusion and function, enhancing the clinical utility of stress myocardial perfusion imaging.

Aged↗