Cardiogenic shock caused by right ventricular infarction: a report from the SHOCK registry

OBJECTIVES: The purpose of this study was to determine the characteristics and outcomes of patients with acute myocardial infarction (MI) complicated by cardiogenic shock due to predominant right ventricular (RV) infarction. BACKGROUND: Although RV infarction has been shown to have favorable long-term outcomes, the influence of RV infarction on mortality in cardiogenic shock is unknown. METHODS: We evaluated 933 patients in cardiogenic shock due to predominant RV (n = 49) or left ventricular (LV) failure (n = 884) in the SHould we emergently revascularize Occluded coronaries for Cardiogenic shocK? (SHOCK) trial registry. RESULTS: Patients with predominant RV shock were younger, with a lower prevalence of previous MI (25.5 vs. 40.1%, p = 0.047), anterior MI, and multivessel disease (34.8 vs. 77.8%, p < 0.001) and a shorter median time between the index MI and the diagnosis of shock (2.9 vs. 6.2 h, p = 0.003) in comparison to patients with LV shock. In-hospital mortality was 53.1% versus 60.8% (p = 0.296) for patients with predominant RV and LV shock, respectively, and the influence of revascularization on mortality was not different between groups. Multivariate analysis revealed that RV shock was not an independent predictor of lower in-hospital mortality (odds ratio 1.07, 95% confidence interval 0.54 to 2.13). CONCLUSIONS: Despite the younger age, lower rate of anterior MI, and higher prevalence of single-vessel coronary disease of RV compared with LV shock patients, and their similar benefit from revascularization, mortality is unexpectedly high in patients with predominant RV shock and similar to patients with LV shock.     

Comparison of late survival in patients with cardiogenic shock due to right ventricular infarction versus left ventricular pump failure following primary percutaneous coronary intervention for ST-elevation acute myocardial infarction

This study compared late survival after primary percutaneous coronary intervention (PCI) in patients with cardiogenic shock due to right ventricular (RV) infarction versus left ventricular (LV) pump failure. Consecutive patients with ST-elevation myocardial infarction treated with primary PCI (n = 2,496) were prospectively enrolled in a registry from 1984 to 2004. Cardiogenic shock occurred before PCI in 189 patients (7.6%). Shock was attributed to predominant RV infarction when there was right coronary artery occlusion with preserved LV function and increased right atrial pressure. Patients with shock due to RV infarction (n = 30) versus LV pump failure (n = 136) had fewer previous infarctions (10% vs 29%, p = 0.03), less multivessel disease (20% vs 47%, p = 0.007), higher right atrial pressure (21 vs 16 mm, p = 0.003), and better LV ejection fraction (57% vs 32%, p <0.001). In-hospital mortality was lower with shock due to RV infarction (23% vs 50%, p = 0.01), and shock due to RV infarction was a significant independent predictor of late cardiac survival (hazard ratio 0.28, 95% confidence interval 0.13 to 0.62, p = 0.002). In conclusion, survival after primary PCI in patients with shock due to RV infarction is better than that in patients with shock due to LV pump failure. This is in contrast to most previous reports. Improved survival is likely related to lower risk profile and previously documented substantial recovery of RV function after primary PCI.     

Predictors of right ventricular dysfunction in patients with coronary artery disease and reduced left ventricular ejection fraction

BACKGROUND: The frequency and determinants of right ventricular (RV) dysfunction in patients with coronary artery disease (CAD) and reduced left ventricular (LV) function have not been thoroughly investigated. METHODS: The study population consists of 80 consecutive patients, invasively evaluated at our centre. Entry criteria were: LV ejection fraction < 45%; angiographic evidence of obstructive CAD; disease history of more than 3 months' duration. Exclusion criteria were: recent myocardial infarction and unstable angina. All patients underwent cardiac catheterization with coronary, LV and RV angiography. RV dysfunction was defined as a RV ejection fraction < 35%, which corresponds to the mean-three standard deviations of controls. RESULTS: Sixty-five patients (81%) had multi-vessel disease and 57 (71%) had a previous myocardial infarction. Mean LV ejection fraction was 31 +/- 8%. Mean RV ejection fraction was 46 +/- 11%. Right ventricular dysfunction was present in 14 patients (18%). An occluded proximal right coronary artery was associated with significantly lower RV ejection fraction (38 +/- 12% versus 47 +/- 10%; P = 0.009) but not LV ejection fraction (30 +/- 8% versus 32 +/- 9%; P = 0.444). However, at multivariate analysis, only pulmonary hypertension was an independent significant predictor of RV dysfunction (P < 0.001; OR: 1.13; CI: 1.06 -1.22). CONCLUSION: Right ventricular dysfunction in patients with chronic ischaemic LV dysfunction is detected in less than 20% of cases. Proximal right coronary artery occlusion is associated with a reduced RV ejection fraction. However, the role of right coronary artery disease is overwhelmed by the haemodynamic burden of pulmonary hypertension, which represents the only independent predictor of RV dysfunction in our population.     

Relationship between radionuclide right ventricular ejection fraction and clinical status in patients with left ventricular dysfunction after myocardial infarction.

OBJECTIVE: To evaluate the influence of right ventricular (RV) function, determined by RV ejection fraction, on the clinical status of patients with ischemic heart disease and left ventricular (LV) EF under 40%. BACKGROUND: The role of RV function as a marker of prognosis in heart failure has been debated. We hypothesized that the degree of RV dysfunction is a determinant of the clinical status and outcome of patients with LV dysfunction after myocardial infarction. PATIENTS AND METHODS: 30 patients, 25 male, with previous myocardial infarction, more than 6 months age, were studied by equilibrium radionuclide angiography. Functional capacity was evaluated by cardiopulmonary exercise test with Naughton protocol. Patients were followed during a 12 month period for major clinical events: death or hospitalisation for congestive heart failure. Two groups of patients were considered according the value of RVEF (< or = 30% and > 30%). RESULTS: The values of EF were: LV = 25 +/- 7% and RV = 35 +/- 9%. Maximum oxygen consumption correlated with RVEF (r = 0.78, p < 0.001) but not with LVEF (r = 0.12, NS). The group of patients with RVEF > 30% had a greater exercise time (712 +/- 229 versus 441 +/- 208 seconds, p = 0.003), higher oxygen consumption (19.8 +/- 5.3 versus 13.5 +/- 3.3 ml/kg/min, p = 0.001) and oxygen consumption in relation to the maximum predicted for age and sex (71 +/- 19 versus 50 +/- 13%, p = 0.002). Cumulative frequency of major clinical events was greater in the group with RVEF < or = 30% (58% vs 6%, relative risk 3.14, 95% CI 1.23 to 5.05). There was no correlation between the values of LVEF and outcome. CONCLUSIONS: In this setting of ischemic LV dysfunction, the RVEF correlates with functional capacity in cardio-pulmonary exercise test and the presence of RV dysfunction is associated to a higher incidence of clinical events.     

Study of shock with normal pulmonary capillary pressure caused by right ventricular failure in acute myocardial infarction]

Of 698 cases of acute myocardial infarction (AMI), 65 cases of cardiogenic shock underwent haemodynamic study. 25 cases had pulmonary capillary pressures (PCP) less than 14 mmHg, 15 of which responded favourably to vascular filling. None of these cases died in a state of shock. In comparison with cardiogenic shock with PCP equal to or greater than 14 mmHg, these 25 patients showed the following features: 1) electrocardiography usually showed posterior or inferior infarction; 2) a higher incidence of right ventricular (RV) involvement; 3) left ventricular (LV) function was relatively unaffected; 4) haemodynamic criteria of RV infarction were demonstrated in most cases. In the absence of causes of hypovolaemia, AMI involving mainly the RV may lead to circulatory failure with normal LV filling pressures and responds favourably to vascular filling. When diagnosed and treated correctly this form of cardiogenic shock has a much lower mortality than usually associated with cardiogenic shock caused by AMI (28 p. 100 compared to 87.5 p. 100 in our series).     

Reduced right ventricular ejection fraction as a marker for idiopathic dilated cardiomyopathy compared with ischemic left ventricular dysfunction.

BACKGROUND: Evidence for the role of right ventricular (RV) function is emerging in patients with heart failure of different etiologies. Studies conducted in dilated cardiomyopathy (IDC) showed a high prevalence of RV dysfunction unrelated to the severity of pulmonary hypertension. The aim of the study was to investigate the role of RV dysfunction in ischemic versus nonischemic patients. METHODS: A series of 153 patients with left ventricular (LV) dysfunction (defined as a LV ejection fraction <45%) of either ischemic (n = 61, coronary artery disease [CAD] group) or nonischemic (n = 92, IDC group) origin were studied invasively. Besides routine catheterization data, RV volumes and ejection fractions were obtained angiographically. Reference data were collected in a control group of healthy subjects. RV dysfunction was defined as a RV ejection fraction <35% and ventricular concordance as a <10% difference between RV and LV ejection fraction. The LV/RV end-diastolic volume ratio was calculated to assess the relative dilatation of the ventricular chambers. Hemodynamic and angiographic data were compared in the 2 groups by univariate and multivariate logistic regression analysis. RESULTS: Patients with IDC and CAD had comparable LV ejection fractions (29% +/- 3% vs 31% +/- 8%, P not significant) and mean pulmonary pressures (27 +/- 12 mm Hg vs 26 +/- 11 mm Hg, P not significant); the LV/RV end-diastolic volume ratio was identical in the 2 groups (1.26 +/- 0.4 vs 1.24 +/- 0.4, P not significant). RV ejection fraction was significantly lower in IDC compared with CAD (33% +/- 10 % vs 46% +/- 11%, P <.0001), with a prevalence of RV dysfunction in the IDC group of 65% compared with 16% in the CAD group (P <.0001); similarly, the prevalence of ejection fraction concordance was 74% versus 33%, respectively (P <.0001). At multivariate analysis, a low RV ejection fraction was a powerful independent predictor of IDC compared with CAD (odds ratio 0.91, 95% confidence interval 0.87-0.94, P <.0001). RV dysfunction had a positive predictive value of 75% and a negative predictive value of 78% for the diagnosis of IDC; for ventricular concordance, these values were 81% and 69%, respectively. The correlation between mean pulmonary artery pressure and RV ejection fraction was weaker in the IDC group compared with the CAD group (R(2) = 0.032, P =.047 and R(2) = 0.172,P <.0001, respectively). CONCLUSION: In the presence of LV dysfunction, a reduced RV ejection fraction is a powerful marker for IDC compared with CAD, independent of age, pulmonary hypertension, LV function, and ventricular dimensions. These findings support the concept that IDC is frequently characterized by a biventricular involvement and that the presence of RV dysfunction represents a distinguishing feature of this disease.     

Pseudonormalized Doppler total ejection isovolume (Tei) index in patients with right ventricular acute myocardial infarction

The Doppler total ejection isovolume (Tei) index is useful for estimating global cardiac function. However, the relation between the right ventricular (RV) Tei index and RV infarction has not been investigated. The relation between the RV Tei index and severity of RV infarction was evaluated in 25 patients with inferior wall acute myocardial infarction (13 with and 12 without RV infarction). RV infarction was diagnosed when right atrial pressure was > or = 10 mm Hg or when right atrial pressure/pulmonary capillary wedge pressure was >0.8 by catheterization. The RV Tei index was significantly increased in patients with RV infarction compared with those without (0.53 +/- 0.15 vs 0.38 +/- 0.14, p <0.05). The RV Tei index in patients with severe RV infarction (right atrial pressure > or = 15 mm Hg) was significantly smaller compared with those with mild/moderate RV infarction (right atrial pressure <15 mm Hg) and showed no significant difference in patients with myocardial infarction but without RV infarction (0.44 +/- 0.09 vs 0.61 +/- 0.16 vs 0.38 +/- 0.14, severe RV infarction vs mild/moderate RV infarction vs no RV infarction, p <0.01). The RV Tei index is generally increased in patients with RV infarction; however, severe RV infarction can be manifested with limited or no increase in the Tei index (pseudonormalization).     

Prognostic significance of persistent right ventricular dysfunction as assessed by radionuclide angiocardiography in patients with inferior wall acute myocardial infarction

We evaluated cardiac hemodynamics and long-term prognosis in patients with right ventricular (RV) acute myocardial infarction (AMI) using Fourier phase and amplitude analysis of radionuclide angiocardiographic scanning. In 143 patients with RV AMI, delayed phase and low amplitude in radionuclide RV images persisted in 54 patients (persistent RV dysfunction group) 3 months after AMI, but disappeared in the remaining 89 patients (improved RV function group). No significant differences were present in RV dimensions, left ventricular (LV) wall motion, LV ejection fraction, or RV ejection fraction between these groups during the acute phase. At 3 months, RV dimension and LV and RV wall motion indexes were significantly higher (p = 0.0292, p = 0.0124, p<0.0001, respectively), and LV and RV ejection fractions were lower (p = 0. 0174 and p = 0.0008, respectively) in the persistent RV dysfunction group. Percutaneous transluminal coronary angioplasty in the acute phase was performed in a smaller group of patients (15% vs. 34%, p = 0.0223), and the degree of residual stenosis in the proximal right coronary artery was significantly greater in the persistent RV dysfunction group than in the improved RV function group (82+/-22% vs. 53+/-30%, p<0.0001). The 8-year survival rate was significantly lower in the persistent RV dysfunction group (p<0.0001). Persistent abnormality of phase and amplitude in radionuclide RV images was a significant independent predictor of long-term survival (odds ratio 10.42; 95% confidence interval 3.65 to 29.71; p<0.0001). Radionuclide angiocardiographic Fourier phase and amplitude scanning can detect persistent RV dysfunction in patients with RV AMI and can predict patient outcome.     

Evaluation of biventricular involvement in hypotensive patients with transmural inferior infarction by two-dimensional echocardiography

Hypotension in inferior myocardial infarction (IMI) may be due to extensive involvement of the right ventricle (RV), left ventricle (LV), or both. We verified this hypothesis in 24 patients with IMI and hypotension (systolic blood pressure less than 100 mm Hg), within 48 hours of admission, by means of two-dimensional echocardiography (2DE). We measured the extent of regional RV and LV asynergy (akinesis and/or dyskinesis) in parasternal short-axis sections at mitral, chordal, midpapillary muscle, and low papillary muscle levels. Initial right heart catheterization revealed predominant RV dysfunction in 16 patients (group 1) and predominant LV dysfunction in eight patients (group 2). For all patients, the initial 2DE revealed: (1) biventricular asynergy involving the posterior RV, posterior LV, and posterior interventricular septum; (2) a wide range of values for the extent of asynergy (RV 21% to 90%; LV 19% to 48%); and (3) a direct correlation between peak creatine kinase levels and percentage of LV asynergy (r = 0.80, p less than 0.001) or percentage of RV plus LV asynergy (r = 0.72, p less than 0.001). Although the extent of LV asynergy was similar in the two groups (34% vs 34%, NS), the extent of RV asynergy was greater in group 1 than in group 2 (57% vs 30%, p less than 0.001). More important, the ratio of RV/LV asynergy was greater for group 1 than group 2 (1.75 vs 0.89, p less than 0.001), and this difference in ratios between the two groups was also found in 2DE studies at 10 days and 6 months. A RV/LV asynergy ratio value of 1.1 provided clear separation between the groups. Thus, the RV/LV asynergy ratio on an initial 2DE can clarify the clinical syndrome of hypotension in patients with IMI. An increased asynergy ratio might identify those patients with predominant RV involvement.     

Ventricular pacing lead location alters systemic hemodynamics and left ventricular function in patients with and without reduced ejection fraction.

OBJECTIVES: We compared left ventricular (LV) systolic and diastolic function during right ventricular (RV), LV, and biventricular (BiV) pacing in patients with narrow QRS duration with and without LV dysfunction. BACKGROUND: The optimal RV pacing lead location for patients with a standard indication for ventricular pacing remains controversial. METHODS: Left ventricular pressure and volume data were determined via conductance catheter during electrophysiology study in 31 patients divided into groups with ejection fraction (EF) > or =40% (n = 17) or EF <40% (n = 14). QRS duration was 91 +/- 18 versus 106 +/- 25 ms, respectively (p = NS). Hemodynamic data were recorded during atrial and dual chamber pacing from the RV apex, RV free wall, RV septum, LV free wall, and BiV. RESULTS: In patients with EF > or =40%, RV pacing at 1 or more sites, but not LV free wall or BiV pacing, significantly (p < 0.05) impaired cardiac output (CO), stroke work (SW), EF, and LV relaxation compared with atrial overdrive pacing. Right ventricular pacing also impaired hemodynamics and LV function in patients with EF <40%. However, LV and BiV pacing increased CO, SW, EF, and LV +dP/dt(MAX) in patients with LV dysfunction. Left ventricular and BiV pacing enhanced an index of global LV cycle efficiency in patients with depressed EF. The detrimental hemodynamic effects of RV pacing were attenuated by selecting the optimal RV pacing site. CONCLUSIONS: Right ventricular pacing worsens LV function in patients with and without LV dysfunction unless the RV pacing site is optimized. Left ventricular and BiV pacing preserve LV function in patients with EF >40% and improve function in patients with EF <40% despite no clinical indication for BiV pacing.     

Left and right ventricular function in inferior acute myocardial infarction and significance of advanced atrioventricular block

Of 139 consecutive patients with a first inferior acute myocardial infarction, 26 (19%) had advanced atrioventricular (AV) block and 113 (81%) did not. All were evaluated by 2-dimensional echocardiography (2-D echo) and radionuclide angiography. Patients with advanced AV block had lower radionuclide left ventricular (LV) ejection fraction (51 +/- 10 vs 58 +/- 11%, p less than 0.01), higher LV wall motion score on 2-D echo (5.6 +/- 2.6 vs 3.1 +/- 2.7, p less than 0.001), lower radionuclide right ventricular (RV) ejection fraction (32 +/- 15 vs 39 +/- 16%, p less than 0.001) and higher RV wall motion score on 2-D echo (3.4 +/- 1.7 vs 1.5 +/- 2, p less than 0.002) than did patients without AV block. The incidence rate of RV dysfunction was higher in patients with advanced AV block (78 vs 40%, p less than 0.02), and the mortality rate was also higher (although not significantly) in patients with advanced AV block (15 vs 6%). In conclusion, patients with inferior acute myocardial infarction and advanced AV block have larger infarct sizes (as seen on radionuclide angiography and 2-D echo) and lower RV and LV function than patients without AV block. This finding may explain the higher mortality rate observed in this group.     

Right ventricular strain and strain rate properties in patients with right ventricular myocardial infarction

BACKGROUND: This study was planned to assess strain and strain rate properties of right ventricle in patients with RV myocardial infarction. MATERIAL AND METHOD: Thirty patients with acute inferior myocardial infarction were included in this study. The presence of right ventricular infarction in association with an inferior myocardial infarction was defined by an ST-segment elevation 0.1 mV in lead V4 R. According to this definition, 15 patients had electrocardiographic signs of inferior myocardial infarction without right ventricular infarction (group I), and 15 patients had electrocardiographic signs of inferior myocardial infarction with right ventricular infarction (group II). Echocardiography was performed using a Vivid 5 System (GE Ultrasound; Horten, Norway) and a 2.5-MHz transducer. 2-dimensional color doppler myocardial imaging (CDMI) data for longitudinal function were recorded from the RV free wall using standard apical view. Offline analysis of the myocardial color Doppler data for regional velocity (V), strain rate (Sr), and strain (S) curves was performed using a special software program (EchoPac 6.4 Vingmed, Horten, Norway). They were assessed in basal, middle and apical segments of the RV. The differences between different groups were assessed with the Mann-Whitney U-test. A value of P < 0.05 was considered statistically significant. RESULTS: Systolic tissue velocity, strain, strain rate of basal (4.8 +/- 0.8 cm/s vs 6.5 +/- 1.2 cm/s, -12 +/- 3% vs -24 +/- 5%, 1.28 +/- 0.3/s vs -1.9 +/- 0.4/s; P < 0.001, <0.001, <0.001, respectively) and mid (4.2 +/- 0.5 cm/s vs 5.4 +/- 0.5 cm/s, -16 +/-3% vs -26 +/- 4%, -1.2 +/- 0.3/s vs -2.1 +/- 0.3/s; P < 0.001, <0.001, <0.001, respectively) segments of right ventricle were significantly lower in patients with RV infarction than in patients without RV infarction. There were no differences between groups for apical strain, strain rate, and systolic tissue velocity. CONCLUSION: This study demonstrates that right ventricular strain and strain rate were lower in patients with left ventricular inferior wall myocardial infarction with, compared to without, right ventricular infarction.     

Contraction pattern of the systemic right ventricle shift from longitudinal to circumferential shortening and absent global ventricular torsion.

OBJECTIVES: The aim of the present study was to characterize the contraction pattern of the systemic right ventricle (RV). BACKGROUND: Reduced longitudinal function of the systemic RV compared with the normal RV has been interpreted as ventricular dysfunction. However, longitudinal shortening represents only one aspect of myocardial deformation, and changes in contraction in other dimensions have not previously been described. METHODS: Fourteen Senning-operated patients age 18.4 +/- 0.9 years (mean +/- SD) with transposition of the great arteries were studied. We compared the contraction pattern of the systemic RV with findings in the RV and left ventricle (LV) of normal subjects (n = 14) using tissue Doppler imaging and magnetic resonance imaging. RESULTS: In the systemic RV free wall, circumferential strain exceeded longitudinal strain (-23.3 +/- 3.4% vs. -15.0 +/- 3.0%, p < 0.001) as was also the case in the normal LV (-25.7 +/- 3.1% vs. -16.5 +/- 1.7%, p < 0.001), opposite from the findings in the normal RV (-15.8 +/- 1.3% vs. -30.7 +/- 3.3%, p < 0.001). Strain in the interventricular septum did not differ from normal. Ventricular torsion was essentially absent in the systemic RV (0.3 +/- 1.8 degrees ), in contrast to a torsion of 16.7 +/- 4.8 degrees in the normal LV (p < 0.001). CONCLUSIONS: In the systemic RV as in the normal LV, there was predominant circumferential over longitudinal free wall shortening, opposite from findings in the normal RV. This may represent an adaptive response to the systemic load. Noticeably, however, the systemic RV did not display torsion as found in the normal LV.     

Right ventricular infarction

Opinion statement  

Response of hypertrophic heart myocardial glycogen to GIK and hypovolemic shock

Glucose-insulin-potassium (GIK) given during myocardial ischemia or anoxemia results in improved myocardial function and augments energy reserves of myocardial glycogen (MG). Because many patients with heart disease also have myocardial hypertrophy, our purpose was to examine whether similar elevations in MG can occur in hypertrophic hearts with GIK administration and to study the effect of hypovolemic shock on those MG levels. Mongrel dogs (n = 5) with myocardial hypertrophy underwent serial myocardial biopsies of the left (LV) and right (RV) ventricles, and blood samples were followed by GIK infusion (14.5 ml/kg/hr) for 2 hr. after which the dogs were subjected to 2 hr of hypovolemic shock (mean arterial pressure = 40 mmHg). It was found that after GIK infusion MG was consistently elevated in both RV (.43 +/- .02 to .60 +/- .04 g%) and LV (.63 +/- .07 to .71 +/- .01 g%) and FFA declined (.20 +/- .05 to .05-.01 mEq/liter). The MG responded to hypovolemia by further significant elevations (RV 1.16 +/- .33; LV .82 +/- .17), as did FFA (.38 +/- .21). These results indicate that hypertrophic hearts can indeed respond to GIK infusion by increasing MG in both the RV and LV, as do normal hearts. These hearts then submitted to hypovolemic shock showed a further elevation of MG. The elevated insulin levels post-GIK resulted in suppression of FFA. Thus GIK administration may have a sparing effect on energy stores of the heart during hypovolemic shock, which could have clinical implications in the treatment of patients with hypertrophic myocardia.     

Exercise-induced ST-elevation is related to left ventricular dysfunction but not to myocardial viability in patients with healed myocardial infarction.

BACKGROUND: Exercise-induced ST-segment elevation was proposed as a marker of myocardial viability after a recent myocardial infarction. AIMS: The aim of this study was to evaluate whether exercise-induced ST segment elevation is related to viability or to left ventricular dysfunction in patients with history of old Q wave myocardial infarction. METHODS: Fifty patients (43 men, age 57+/-11 years) were studied 31+/-49 months after a Q wave myocardial infarction. They all underwent stress, reinjection-redistribution, and late redistribution Tl-201 SPECT, completed by equilibrium radionuclide angiography. Viability was defined by defect reversibility or significant (>60%) persistent Tl-201 uptake in dyssinergic segments on late redistribution SPECT. Relative post-exercise and reinjection-redistribution LV volumes were calculated using validated software (QGS). RESULTS: Twenty-one out of 50 patients (42%, G1) had significant stress-induced ST-elevation (>1 mm 80 ms after J point in at least 2 ECG leads with Q wave), and 29/50 (58%, G2) did not. Seventeen out of 50 patients (34%) demonstrated myocardial viability on late redistribution scan. The diagnostic accuracy of exercise-induced ST-elevation was only 52% for viability assessment. Significant LVEF reduction and increased relative LV volumes were observed in G1 compared to G2 (LVEF: 39+/-10% vs. 49+/-11%, P=0.003; post-stress LV volume: 134+/-98 ml vs. 81+/-41 ml, P<0.02; reinjection-redistribution LV volume: 123+/-86 ml vs. 79+/-40 ml; P<0.02). Perfusion defects were similar in G1 and G2 (post-exercise: 38+/-12% vs. 37+/-14%, ns; reinjection-redistribution: 31+/-11% vs. 30+/-11%, ns; late redistribution: 30+/-10% vs. 28+/-11%, ns). CONCLUSION: These results suggest that, in patients with history of myocardial infarction, exercise-induced ST-segment elevation is not related to persistent myocardial viability but is associated to left ventricular dysfunction.     

Assessment of right ventricular function in acute inferior myocardial infarction using 133-xenon imaging

The detection of right ventricular dysfunction in acute inferior myocardial infarction is important because of its potentially serious consequences which may be remediable with the appropriate therapeutic manoeuvres. A technique has been developed to assess right ventricular function using 133-xenon. This technique was applied to 26 patients who had sustained an acute inferior myocardial infarction. Right ventricular ejection fractions ranged from 7-54%, mean 30 +/- 11%, which was significantly lower than values obtained from normal volunteers (n = 21), mean 43 +/- 5%, and patients with arteriographically proven coronary artery disease without previous myocardial infarction (n = 12), mean 39 +/- 9%, P less than 0.001, and P less than 0.001, respectively. In the patients with acute inferior myocardial infarction 18 patients (69%) had evidence of right ventricular dysfunction (right ventricular ejection fraction less than 35%). 13/26 patients (50%) had clinical evidence of right ventricular dysfunction with a mean right ventricular ejection fraction 26 +/- 11% (range 7-54%) which was significantly lower than the patients without evidence of right ventricular dysfunction, mean 35 +/- 9% (range 16-49%), P less than 0.001. The clinical signs had a sensitivity of 72% (13/18), a specificity of 87.5% (7/8) and a predictive accuracy of 76% (20/26) when compared to the imaging data. In conclusion: (1) gated 133-xenon imaging provides a method for assessing right ventricular function in the setting of acute myocardial infarction; (2) a wide spectrum of right ventricular dysfunction occurs following inferior myocardial infarction which may not manifest itself clinically.     

Myocardial performance index in evaluation of acute right ventricular myocardial infarction

The goal of this study was to evaluate the role of Doppler time interval-derived myocardial performance index (MPI) in the setting of acute right ventricular myocardial infarction (RVMI). Inferior myocardial infarction is accompanied by RVMI in over a third of cases. We do not have easily applicable noninvasive tools for reliably quantifying the right ventricular (RV) dysfunction in RVMI and to serially follow alterations. Clinical and echocardiography data of all acute inferior myocardial infarction (IMI) admissions (n = 135) to our referral teaching institute were prospectively collected for the study. After exclusions, study group comprised of 36 patients with RVMI diagnosed by >/=1 mm ST segment elevation in V3R-V5R of right-sided ECG and 63 patients without RVMI constituted the control group. All patients underwent echocardiography within 24 hours of admission. Normal range of MPI for our laboratory was estimated from 50 age-matched healthy subjects. RV MPI was elevated to a mean of 0.53 +/- 0.22 in RVMI (Normal MPI 0.20 +/- 0.05, P-value < 0.001). IMI without RVMI did not elevate MPI significantly (0.21 +/- 0.17, P-value NS). Repeat MPI estimation in 11 RVMI (7 thrombolyzed) patients after 5 days showed dramatic reduction (0.23 +/- 0.12, P-value < 0.001). This reduction was noted irrespective of thrombolysis. RV MPI >/= 0.30 has high sensitivity (82%) and specificity (95%) for the diagnosis of RVMI in the presence of acute IMI. MPI can reliably diagnose RV infarction. It can be used to quantify right ventricular dysfunction and assess acute improvements in RV function.     

Left ventricular pressure effects on right ventricular pressure and volume outflow

Massive destruction of the right ventricular free wall has been shown to cause only mild hemodynamic alterations. Further, the derivative of right ventricular (RV) pressure (P) is broad or double peaked, with one peak occurring coincidentally with peak left ventricular (LV) dP/dt. Both observations suggest a direct LV assistance to RV function. Since the ventricles contract nearly simultaneously, the relative contribution of LV to RV pump function has been difficult to determine. This LV assistance was quantified in six canine experiments using a unique electrically isolated RV preparation. While on total cardiopulmonary bypass, the RV free wall was electrically isolated from the remainder of the heart. This preparation allowed for wide variations in the timing interval between RV and LV contractions. Double-peaked waveforms for RVP and pulmonary flow (RVF) occurred over a wide range (0 to 300 ms) of pacing intervals between the RV and LV. One derivative peak always followed RV contraction for RVP and RVF (r = 0.971 +/- .011, P less than 0.01: r = 0.972 +/- .012, p less than 0.01; respectively). The second derivative peak was unrelated to the RA-RV pacing interval (r = 0.297 +/- .191, P greater than 0.5 RVP; 4 = 0.237 +/- .278, P greater than 0.5 RVF), but corresponded to the maximal LVP rise. Additionally, the magnitude of the two derivative peaks was similar when the ventricles contracted synchronously. When RV contraction preceded or followed LV contraction, the derivative peak associated with LV contraction was significantly greater (P less than 0.05, range 2.1 +/- 0.6 to 6.7 +/- 1.6 for RVP; P less than 0.05 range 1.9 +/- 0.4 to 6.7 +/- 1.5 for RVF) than the derivative associated with RV contraction. These data demonstrate a normally present, large LV assistance to RV contraction and may help to explain the RV response to myocardial infarction.     

Effect of antecedent systemic hypertension on subsequent left ventricular dilation after acute myocardial infarction (from the Survival and Ventricular Enlargement trial)

Whether antecedent systemic hypertension influences the risk of subsequent left ventricular (LV) dilation in patients after an acute myocardial infarction with LV systolic dysfunction is unclear. We assessed echocardiographic evidence of ventricular remodeling from baseline (mean +/- SD 11 +/- 3 days) to 2 years after an acute myocardial infarction in 122 hypertensive (defined as a history of treated hypertension, baseline systolic blood pressure > or =140 or baseline diastolic blood pressure > or =90 mm Hg) and 334 nonhypertensive patients in the Survival and Ventricular Enlargement echocardiographic substudy. Compared with nonhypertensives, baseline heart size, defined as the sum of the average short- and long-axis LV cavity areas, was similar (70.1 +/- 11.9 vs 68.8 +/- 11.2 cm(2), p = 0.33 at end-diastole; 50.1 +/- 11.3 vs 48.8 +/- 10.8 cm(2), p = 0.31 at end-systole), but short-axis LV myocardial area (24.7 +/- 4.3 vs 25.7 +/- 5.0 cm(2), p = 0.043) and wall thickness (1.15 +/- 0.16 vs 1.21 +/- 0.17 cm, p = 0.004) at end-diastole were greater among hypertensives. The myocardial infarct segment lengths were similar in the 2 groups (p = 0.22). Although LV cavity areas increased significantly in the 2 groups from baseline to 2 years (p < or =0.001), the increase was significantly greater in hypertensives than in nonhypertensives (+5.6 +/- 11.5 vs +2.2 +/- 10.7 cm(2), p = 0.005 at end-diastole; +6.23 +/- 12.75 vs +2.94 +/- 11.4 cm(2), p = 0.012 at end-systole). There was no concomitant difference in the change in LV myocardial area or LV wall thickness between the 2 groups (p >0.30). After adjusting for known confounders, antecedent hypertension was associated with a doubling of the risk of LV dilation (50.8% vs 37.7%, odds ratio 2.09, 95% confidence interval 1.27 to 3.45, p = 0.004). This association was not modified by diabetes mellitus, myocardial infarct segment length, or captopril use (all p values for interaction >0.10). We conclude that antecedent hypertension is associated with subsequent LV dilation in patients after acute myocardial infarction with LV systolic dysfunction.