Collateral vessel development after right ventricular infarction in the pig

Although the right coronary artery supplies both ventricles in the pig, a gradual proximal right coronary occlusion produces infarction in the left ventricle, whereas the right ventricle is usually spared. This study evaluates the influence of right ventricular hypertension and hypertrophy (RVHH) on the occurrence of right ventricular infarction and the difference in the rate and extent of collateral vessel development after gradual right coronary occlusion in pigs with (RVHH group) and without (control group) increased right ventricular pressure and mass. Right ventricular hypertension and hypertrophy were induced by pulmonary arterial banding which raised right ventricular systolic pressure from 24 to 74 mm Hg and doubled right ventricular mass in 4 weeks. Right coronary occlusion was produced with an ameroid constrictor in 24 control group pigs and 15 RVHH pigs. Serial selective coronary cineangiograms on days 4, 8, 14, 21 and 28 after ameroid constrictor placement showed no difference in first appearance of collateralization to the occluded right coronary artery. Total collateralization, which was present in all pigs studied in the control group by days 21 and 28, was present in only 57 percent of the RVHH group at the same time. Although left ventricular infarction occurred in all animals in both groups, right ventricular infarction was not found in the control group but was seen in 80 percent of the RVHH group. There was no correlation between the degree of collateralization seen and the size of the right ventricular infarction found. Experimentally induced right ventricular hypertrophy and hypertension make the right ventricle susceptible to infarction and impeded total collateral filling of the occluded right coronary artery in some of the animals studied.     

Biventricular dynamics during quantitated anteroseptal infarction in the porcine heart.

The porcine heart has been shown to have close anatomic similarity to the human heart and was used as the experimental model in this study to gain further understanding of the early responses of both ventricles during acute anteroseptal myocardial infarction. High fidelity pressure and flow data were measured and multiple preejection and ejection variables were calculated for both ventricles. Infarct weight and distribution in both ventricles were quantitated. The standard infarction resulted from single stage ligation of the left anterior descending coronary artery just beyond its midpoint and second left ventricular branch. It comprised an average of 15.8 percent of total ventricular myocardium with an infarct/perfused ratio of 0.62 and a periinfarction transition zone of 7.5 mm, and involved significant portions of both ventricles and the interventricular septum. Performance characteristics of both ventricles were altered significantly by anteroseptal infarction and involved all phases of contraction--end-diastole, isovolumic systole and ventricular ejection. Although contractile alterations in the right ventricle were significant, they were somewhat delayed, yielding relatively low correlation coefficients with analogous left ventricular contractile indexes. These correlations became quite distinct during specific ventricular stresses. Comparison of anterolateral and anteroseptal infarction, matched in terms of infarct size, indicated that the right ventricular changes in the latter were related to direct involvement of the right ventricular free wall and septum rather than secondary to left ventricular alterations.     

Differential effects of left anterior descending coronary occlusion on left and right ventricular anterior wall thickening in the conscious pig.

OBJECTIVE: In humans, the left anterior descending coronary artery supplies the left ventricular wall, anterior septum and the paraseptal part of the right ventricular anterior wall. Our aim was to study the effects of acute left anterior descending coronary occlusion on wall thickening in the regions of the left and right ventricular anterior walls supplied by the artery, and in remote, non-ischaemic regions of both ventricles. METHODS: Systolic wall thickening (defined as percent thickening with respect to end diastolic wall thickness) was studied in eight conscious pigs every 15 s during 1 min of acute left anterior descending coronary occlusion by a cuff occluder, and every 30 s during 4 min of reperfusion. Pigs were instrumented with ultrasonic microcrystals measuring wall thickness in the anterior walls (left anterior descending artery territory) and lateral walls (left circumflex or right coronary artery territory) of both ventricles, and a left ventricular pressure microtransducer. RESULTS: During control and reperfusion, both anterior walls displayed similar systolic thickening. During coronary occlusion, the left ventricular anterior wall showed paradoxical systolic thinning (dyskinesia) whereas the right ventricular anterior wall showed only hypokinesia. CONCLUSIONS: In the presence of equal blood flow deprivation, the right ventricular anterior wall supplied by the left anterior descending coronary artery displays a significantly lesser degree of functional impairment than the left ventricular anterior wall supplied by the same artery. This differential effect may be due to mechanical unloading of the right ventricular anterior wall resulting from left ventricular anterior wall ischaemia. This afterload reduction due to decreased mechanical interaction between the two walls would allow the right ventricular anterior wall to express its contractile reserve in the form of systolic thickening.     

Role of two-dimensional echocardiography, pulsed, continuous wave color flow Doppler techniques in the assessment of ventricular septal rupture after myocardial infarction

Two-dimensional echocardiography, pulsed and continuous wave Doppler techniques were used for the evaluation of 15 consecutive patients (9 men, 6 women; mean age 71 years, range 61 to 79) with ventricular septal rupture due to acute myocardial infarction (7 anterior, 8 posterior). Standard and modified off-axis 2-dimensional echocardiographic views from parasternal, apical and subcostal windows correctly identified this defect in 14 of the 15 patients. Pulsed Doppler echocardiography confirmed the presence of left-to-right-sided shunt by showing a high-velocity, aliased, systolic flow and a low-velocity diastolic flow in the right ventricle in 14 patients. Continuous wave Doppler echocardiography showed a high-velocity systolic and low-velocity diastolic flow signal of left-to-right shunt in 14 patients. Color flow Doppler imaging identified a left-to-right shunt in all 6 patients in whom it was performed. Doppler and 2-dimensional echocardiographic studies missed a small apical septal defect in 1 patient with anteroseptal myocardial infarction. Two-dimensional echocardiography correctly diagnosed right ventricular infarction in all 5 patients with posteroinferior infarction. Ventricular septal rupture and/or left-to-right-sided shunt was confirmed in all 15 patients by the following: surgical inspection in 11, necropsy in 3, left ventricular cineangiography in 5 and right-sided heart catheterization and oximetry data in 13 patients. Data indicate that 2-dimensional echocardiography correctly shows the precise location of septal rupture in most patients after acute myocardial infarction and allows assessment of left and right ventricular infarction and function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Impaired right ventricular filling in old myocardial infarction

To evaluate ventricular filling and interactions between right and left ventricles in patients with old myocardial infarction, right and left ventricular time-volume curves were analyzed from a cineangiographic study of 10 normal subjects (Group 1), 10 patients with old anterior myocardial infarction (Group 2) and 10 patients with old inferior myocardial infarction (Group 3). Volumes of both ventricles were calculated from each frame over an entire cardiac cycle using Simpson's method. From time-volume curves, peak ejection rates, peak filling rates and atrial kick rates were obtained for both ventricles and these parameters were normalized by end-diastolic volume. All patients were in sinus rhythm with heart rates less than 80 beats/min. There were no significant differences among the 3 groups in end-diastolic pressure of both ventricles and mean pulmonary artery pressure. Left ventricular ejection fractions were significantly lower in Groups 2 and 3 than in Group 1 (p less than 0.001, p less than 0.005, respectively), although there were no significant differences in end-diastolic volume indexes of either ventricle among the 3 groups. Peak left ventricular ejection rate and peak filling rates of the left and right ventricles were lower in Group 2 than in Group 1 (p less than 0.01, p less than 0.05, p less than 0.01, respectively) and peak filling rate of the right ventricle in Group 2 correlated with the peak filling rate of the left ventricle and left ventricular ejection fraction (r = 0.64, r = 0.64, respectively). Peak filling rate of the right ventricle in Group 2 correlated inversely with left ventricular peak negative dp/dt (r = -0.72), but no correlation was found between peak filling rate of the right ventricle and left ventricular end-diastolic volume index or mean pulmonary artery pressure. Peak ejection rate of the left ventricle and peak filling rates of both ventricles in Group 3 were lower than in Group 1 (p less than 0.02, p less than 0.02, p less than 0.01, respectively) and no correlation was found between peak filling rates of both ventricles. Wall motion of the right ventricular septal portion was slightly reduced in 5 patients in Group 2. In all patients in Group 3, right ventricular wall motion centering around the right ventricular diaphragmatic portion was reduced. These results suggest that in old inferior myocardial infarction, right ventricular wall motion abnormality results in impaired right ventricular filling, whereas in old anterior myocardial infarction, right ventricular filling is reduced indirectly due to impaired left ventricular filling.     

Hypertrophic cardiomyopathy with midventricular and subvalvular obstruction in both heart ventricles

Typical (subaortic) and atypical (midventricular or apical) obstructions of both ventricles in HOCM are rare events. This combination could be demonstrated in a 21-year-old female patient by heart catheterization and angiocardiography. Simultaneous registration via 2 catheters in each ventricle showed pressure gradients with two steps in both ventricles: RV apical/RV midventricular 70-100 mm Hg, RV midventricular/subvalvular 25 mm Hg; LV apical/LV midventricular 70 mm Hg, LV midventricular/LV subvalvular 30 mm Hg; no valvular pressure gradients. Morphology of the obstructions is demonstrated by angiography: severe bilateral septal hypertrophy with midventricular systolic obstruction, systolic obstruction of right ventricular infundibulum by hypertrophy of the crista supraventricularis, systolic apical separation in the right ventricle; stenosis of the left ventricular outflow tract by SAM, systolic apical separation in the left ventricle by hypertrophy of papillary muscles.     

Physiological early diastolic intraventricular pressure gradient is lost during acute myocardial ischemia

A consistent pattern of intraventricular regional pressure gradients exists under physiological conditions during the rapid filling phase of diastole in the normal dog left ventricle. We hypothesized that this pressure gradient pattern is caused, in part, by early diastolic recoil of the left ventricular walls in conjunction with release of elastic potential energy stored during systole, generating suction and thus contributing to diastolic filling. If so, any condition that interferes with normal regional systolic function might be expected to modify the pattern of the normal early diastolic intraventricular pressure gradients. Accordingly, the present study was designed to determine whether acutely induced regional systolic left ventricular mechanical dysfunction is accompanied by changes in the pattern of the early diastolic intraventricular pressure gradients. Acute myocardial ischemia was induced by balloon occlusion of the left anterior descending coronary artery (LAD) in nine anesthetized closed-chest dogs. The maximum early diastolic intraventricular pressure gradient (MIVP) was measured between the mid-left ventricle and apex with a dual-sensor micromanometer (3-cm spacing between the sensors) before and 20 minutes after LAD occlusion. Ejection fraction (EF) and number of dyskinetic chords (DChords) were measured from left ventricular contrast ventriculograms. Twenty minutes after LAD occlusion, the nine dogs evidenced significant changes in EF (56 +/- 10% to 37 +/- 8%), DChords (0 +/- 0 to 17 +/- 16 chords), left ventricular minimum pressure (-1.7 +/- 0.5 to 0.0 +/- 1.5 mm Hg), left ventricular end-diastolic pressure (4.2 +/- 1.2 to 5.9 +/- 2.2 mm Hg), and heart rate (90 +/- 17 to 103 +/- 18 beats/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Involvement and function of the right ventricle in acute myocardial infarct. Hemodynamic, echocardiographic and angioscintigraphic correlations

To assess the acute effects of myocardial infarction on right ventricular function 22 patients were studied utilizing right heart catheterization, radionuclide angiography and two dimensional echocardiography. Thirteen patients had inferior myocardial infarction (Group I) and 9 anteroseptal or anterior (Group II). Hemodynamic findings suggesting right ventricular infarction were present in 3 patients of Group I. Mean radionuclide right ventricular ejection fraction was lower in inferior myocardial patients (38.2 +/- 7.6-Group I vs 50.3 +/- 11.4-Group II, p less than 0.005), while left ventricular ejection fraction in anteroseptal, and anterior myocardial infarction patients (36.8 +/- 10.5-Group II vs 55.9 +/- 7.6-Group I, p less than 0.001). Six patients in Group I presented a depressed radionuclide right ventricular ejection fraction (less than 40%): moreover right ventricular ejection fraction correlated with left ventricular ejection fraction in Group II (r = 0.79, p less than 0.001) but not in Group I (r = 0.55, p = NS). By mean of 2 dimensional echocardiography Group I patients had an increased right ventricular end diastolic area (15.3 +/- 3.8 vs 12.1 +/- 1.2 cm2, p less than 0.05) while Group II an increased right ventricular free wall motion (47.3 +/- 10.7 vs 32.4 +/- 14.1%, p less than 0.005); right ventricular end diastolic area correlated with right ventricular ejection fraction only in Group I (r = 0.60, p less than 0.05). Five patients in Group I and no patients in Group II had an enlarged right ventricular end diastolic area. Therefore, radionuclide and echocardiographic evidence of right ventricular involvement were not always associated with abnormal hemodynamics. Thus, the damaged right ventricular chamber dilates to allow an adequate stroke volume in presence of low ejection fraction; hemodynamic significant right ventricular myocardial infarction becomes evident only in patients with more severe right ventricular compromise; the increase in right ventricular free wall motion in anterior myocardial infarction patients compensates the loss of contribution of interventricular septum contraction.     

Transient Ischemia Does Not Limit Subsequent Ischemic Regional Dysfunction in Humans: A Transesophageal Echocardiographic Study During Minimally Invasive Coronary Artery Bypass Surgery

Objectives. This study sought to assess the effects of sequential coronary artery occlusion during minimally invasive coronary artery bypass graft surgery (CABG) on hemodynamic variables and left ventricular systolic function by means of transesophageal echocardiography (TEE).Background. Clinical and experimental studies suggest a protective effect of ischemic preconditioning in patients with acute coronary syndromes. However, the effect of repetitive myocardial ischemia on myocardial mechanical function in humans is not completely understood.Methods. Seventeen patients with left anterior descending coronary artery (LAD) stenosis ≥70% and normal rest left ventricular systolic function referred for minimally invasive CABG underwent intraoperative TEE for assessment of regional left ventricular wall motion and measurement of hemodynamic variables at baseline (baseline 1), during a 5-min coronary occlusion (occlusion 1), after a 5-min reperfusion period (baseline 2) and a during a second coronary occlusion during bypass anastomosis (occlusion 2).Results. Left ventricular wall motion score (LVWMS) increased significantly from baseline (16.0) to occlusion 1 (21.4 ± 3.1 [mean ± SD], p < 0.05) and occlusion 2 (21.8 ± 3.1, p < 0.05). No difference in LVWMS was noted between occlusions 1 and 2. Pulmonary artery systolic pressure increased significantly from baseline (25 ± 6 mm Hg) to occlusion 1 (32 ± 7 mm Hg, p < 0.05) and occlusion 2 (33 ± 6 mm Hg, p < 0.05). Pulmonary artery diastolic pressure also increased significantly from baseline (12 ± 4 mm Hg) to occlusion 1 (16 ± 4 mm Hg, p < 0.05) and occlusion 2 (16 ± 4 mm Hg, p < 0.05). No significant differences in pulmonary artery pressures were noted between occlusions 1 and 2.Conclusions. Ischemic dysfunction was precipitated by the 5-min LAD occlusion, as shown by the increase in LVWMS and pulmonary artery pressure. However, a 5-min coronary occlusion and the resulting ischemia do not alter regional left ventricular systolic function during subsequent ischemia in humans.     

Effects of restored blood flow on the contractile function of the right ventricle in patients with acute myocardial infarct: data of two-dimensional computerized echocardiography

The volumes of the right and left ventricles were measured in 78 patients with first acute transmural myocardial infarction at days 1, 3, 7, 14, and 28 of the disease. Thirty four patients were diagnosed as having anterior myocardial infarction, 35 presented with inferior myocardial infarction, and 9 had a concurrent right and left ventricular inferior wall myocardial infarction. A high incidence of right ventricular dysfunction was confirmed both in anterior and inferior myocardial infarction. The most profound right ventricular contractile dysfunctions were detected in patients with proximal right coronary occlusion in the absence of reperfusion. Successful thrombolytic therapy for myocardial infarction was found to affect right ventricular function to a lesser extent than left function.     

Long-term effects of xamoterol on left ventricular diastolic function and late remodeling: a study in patients with anterior myocardial infarction and single-vessel disease

The purpose of the study was to examine whether the prolonged administration of the beta 1-adrenoceptor partial agonist xamoterol could improve left ventricular diastolic function and affect the global remodeling process of the left ventricle after anterior myocardial infarction. In 22 patients with anterior myocardial infarction and single-vessel disease, left ventricular angiography (+ Millar) was performed under basal conditions 1 to 2 months after the acute myocardial infarction. Eight patients were then treated for 3 months with placebo and 14 were treated with xamoterol (200 mg bid) and a second left ventricular angiographic study was performed. Angiograms were digitized frame by frame to derive the diastolic pressure-volume relationship and to compute wall stress. An index of elastic myocardial stiffness was computed at a constant stress of 30 kdynes/cm2 before and after treatment. To evaluate changes in left ventricular shape, segmental areas in anterior and inferior segments were computed and compared at end-diastole and end-systole. After xamoterol, left ventricular end-diastolic pressure and mean diastolic wall stress decreased (from 24 +/- 5 to 15 +/- 5 mm Hg and from 57 +/- 32 to 38 +/- 22 kdynes/cm2, respectively; both p less than .01 vs baseline and vs placebo). These changes were accompanied by a downward shift in the diastolic pressure-volume relationship and by a decrease in the index of myocardial stiffness from 526 +/- 270 to 371 +/- 194 kdynes/cm2 (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of left and right ventricular end-systolic pressure-volume relations in congestive heart failure

A hemodynamic-radionuclide study was performed to compare the relations between end-systolic pressure and volume in the left and right ventricles in 10 patients with biventricular failure, and to correlate the end-systolic pressure-volume slope with baseline variables of systolic function. During nitroprusside or nitroglycerin infusion, or a combination of both, linear relations were found between end-systolic pressure and volume for both ventricles. In 9 of 10 patients, the end-systolic pressure-volume slope was greater for the left ventricle (mean +/- SD 1.12 +/- 0.36 mm Hg X m2/ml) than for the right ventricle (0.46 +/- 0.27 mm Hg X m2/ml) (p less than 0.001). In all 10 patients, the volume-axis intercept of the pressure-volume relation was greater for the left ventricle (82 +/- 66 ml/m2) than for the right ventricle (2 +/- 30 ml/m2) (p less than 0.005). Right ventricular pressure-volume slope correlated weakly with baseline right ventricular ejection fraction (r = 0.69, p less than 0.05), strongly with the baseline right ventricular end-systolic pressure-volume ratio (r = 0.89) and inversely with baseline right ventricular end-systolic volume (r = -0.86). In conclusion, 1) in patients with severe biventricular failure, changes in systolic pressure influence end-systolic volume more strongly in the right than in the left ventricle. 2) For the right ventricle, the slope of the end-systolic pressure-volume relation is directly related to rest indexes of systolic function. 3) The greater the end-systolic volume at rest, the greater the predicted improvement in right ventricular emptying for any vasodilator-induced reduction in pulmonary artery end-systolic pressure.     

急诊血运重建对急性心肌梗死左心室功能的影响

目的应用二维超声心动图及多普勒组织成像（Doppler tissue imaging，DTI）评价急诊血运重建（包括静脉溶栓或者急诊冠状动脉支架置入术）对急性心肌梗死（acute myocardial infarction，AMI）左心室收缩和舒张功能的影响。方法入院后根据AMI患者治疗方法分为常规组和治疗组。常规组30例给予内科常规治疗；治疗组20例在内科常规治疗基础上实施静脉溶栓或急诊冠状动脉支架置入术。应用DTI检测左心室射血分数、二尖瓣血流舒张早期流速峰值（peak velocity at early diastole，VE）和舒张晚期流速峰值（peak velocity at late diastole，VA）比值（VE／VA），DTI成像模式检测二尖瓣环后间隔、侧壁、前壁、下壁、前间隔和后壁6个节段的收缩期运动速度峰值（peak velocity during systole，Sa）、舒张早期运动速度峰值（peak velocity at early diastole，Ea）和心房收缩期流速峰值（peak velocitv at atrial contraction，Aa），并计算Ea／Aa比值。各取6个节段的平均值。结果所有AMI患者于发病后1周、3月末左心室射血分数、VE／VA、Sa、Ea和Ea／Aa均较对照组降低；予急诊血运重建的AMI患者于AMI发病后3个月S。和E。较本组发病后1周增高，并较未行急诊血运重建干预组（常规组）发病后3个月增高。结论AMI后左心室收缩和舒张功能受损，实施急诊血运重建可以有效改善心脏功能．应用DTI技术检测二尖瓣环运动速度可以精确反映AMI患者局部节段性心功能的恢复。     

The effects of pressure-induced right ventricular hypertrophy on left ventricular diastolic properties and dynamic geometry in the conscious dog

To determine whether chronic pressure overload and hypertrophy of the right ventricle alter the diastolic properties of the left ventricle, six adult dogs underwent banding of the pulmonary artery and were instrumented for studies 8 months later. Fourteen control dogs were also studied. Pressure and dimension data were collected from the dogs while they were awake and unsedated. The anterior-posterior, septal-free wall, and base-apex axis diameters of the left ventricle were measured with ultrasonic dimension transducers. Right and left ventricular pressures were measured with micromanometers. Pulmonary arterial banding resulted in increased right ventricular/body mass ratios (2.70 +/- 0.36 g/kg vs 1.52 +/- 0.15 g/kg control; p less than or equal to .05) and increased left ventricular/body mass ratios (4.84 +/- 0.64 g/kg vs 4.21 +/- 0.49 g/kg control; p less than or equal to .05). Right ventricular peak systolic and end-diastolic pressures were higher among the banded dogs (50 +/- 20/7 +/- 5 mm Hg vs 31 +/- 6/3 +/- 2 mm Hg control; p less than or equal to .05). A rearrangement in the three-dimensional geometry of diastolic filling occurred in the banded dogs. Extension from unstressed diastolic dimension (strain) in the base-apex axis was significantly larger in the banded dogs at left ventricular transmural pressures of 12, 8, and 4 mm Hg; strains in the septal-free wall axis were significantly smaller at transmural pressures of 12 and 8 mm Hg. Normalized diastolic left ventricular pressure-volume data and midwall circumferential stress-strain data were fit to the Kelvin viscoelastic equation. The normalized pressure-volume relationships of the banded dogs lay significantly to the left of those of the controls, indicating a loss of left ventricular chamber compliance. The midwall circumferential stress-strain relationships of the banded dogs were also shifted to the left, indicating a loss of intrinsic myocardial compliance. Thus, during the course of right ventricular hypertrophy caused by right ventricular pressure overload, alterations in the mass, geometry, and material properties of the left ventricle occur. At 8 months the chamber compliance of the left ventricle is compromised by these changes.     

Echoventriculographic detection, localization, and quantification of left ventricular asynergy in acute myocardial infarction. A correlative echo- and electrocardiographic study.

"Echoventriculography", an echocardiographic method specially developed to scan the regional function of the left ventricle, is introduced for studying left ventricular wall motion alteration in patients with acute myocardial infarction. Purposeful probe directions, a 2:1 magnification, and careful adjustment of the gain and reject levels allowed a direct echocardiographic scanning of practically the entire left ventricle. Technically acceptable echoventriculograms were obtained from the upper and lower halves of the septal, anterior, lateral, and postero-inferior left ventricle segments in all observations on 30 consecutive patients with acute myocardial infarction. Various degrees of regional left ventricular asynergy were present in 100 per cent of the patients with acute myocardial infarction. In contrast, synergic ventricular segmental wall motion was observed in 40 healthy subjects. Pronounced asynergy was already detectable within 12 hours from onset of the symptoms of acute myocardial infarction. Echoventriculography detected acute left ventricular asynergy as well in the anteroseptal or lateral as in the posteroinferior locations. The anterior and/or septal infarction (13 of the 30 patientsy always showed a paradoxical systolic motion of the, generally large, infarcted areas. The amplitude of abnormal outward motion was up to 5 mm. In the posteroinferior infarctions (17 patients) akinetic or hypokinetic modes prevailed. The contractile function of the uninvolved segments could be measured at the same time. Hypercontractile left ventricular wall motion was common in these healthy areas in acute myocardial infarction. These findings provide useful insight into the various components of the overall left ventricular pump function in acute myocardial infarction. The validity of the echoventriculographic evaluations of the segmental left ventricular function subsets was further confirmed in 2 patients undergoing left ventricular cineangiographic studies and in 2 by necropsy. The site of the asynergic left ventricular wall motion abnormalities correlated excellently with electrocardiographic prediction of the site of acute myocardial infarction. The echoventriculographic analysis proved to be more accurate in detecting asynergy than was the electrocardiogram. This new echoventriculographic method may become a useful tool for serial noninvasive alalysis of left ventricular performance, in detecting both the asynergic areas and the reserve function of the normal regions in acute myocardial infarction.     

Right ventricular myocardial infarction with anterior wall left ventricular infarction: an autopsy study

Right ventricular myocardial infarction has been reported to occur exclusively in association with inferior left ventricular infarction. To determine the frequency of right ventricular myocardial infarction in association with anterior left ventricular myocardial infarction, all hearts with anterior myocardial infarction studied over a 3-year period were examined for evidence of right ventricular necrosis or scar. Of 97 hearts with anterior myocardial infarction, 13 (13%) had anterior right ventricular myocardial infarction. The right ventricular infarcts involved from 10% to 50% (mean 28%) of the circumference of the right ventricular free wall from base to apex. The associated left ventricular infarcts were all anteroseptal and large and involved from 36% to 67% (mean 50%) of the total area of the left ventricular free wall and septum. Nine of the 13 patients underwent equilibrium radionuclide angiography and six had demonstrable right ventricular regional and global dysfunction. Thus, right ventricular myocardial infarction does occur with anterior wall left ventricular infarction, and right ventricular dysfunction may be demonstrable by radionuclide angiography. Further investigation is needed to define the hemodynamic characteristics, clinical importance, and therapeutic implications of anterior right ventricular myocardial infarction.     

Right ventricular systolic and diastolic functions assessed by 81mKr scintigraphy and relation to ventricular septal ischemia

Right ventricular (RV) systolic and diastolic functions were assessed in patients with previous anteroseptal myocardial infarction to ascertain the influence of interventricular septal ischemia on RV function. Gated right ventriculography with continuous infusion of krypton-81 m was performed in 12 normal subjects and 28 patients with infarction but without significant stenosis of the right coronary artery. Furthermore, RV contractile reserve by postextrasystolic potentiation was evaluated by gated radionuclide ventriculography with 99mTc-HSA. The patients with anteroseptal infarction were divided into two groups by the presence or absence of three hours' redistribution in the septal region on exercise thallium-201 myocardial scintigraphy. Two indices of systolic function (ejection fraction and the peak ejection rate) and three indices of diastolic function (1/3 diastolic filling rate, the peak filling rate and time to the peak filling rate) were derived from the right ventricular time-activity curve and its derivative curve. There was no difference in systolic function among normal subjects and patients with or without redistribution. However, diastolic function was impaired only in the patients without redistribution. The RV contractile reserve in the patients without redistribution was less than in those with it. Thus, RV systolic function was maintained in the patients with anteroseptal infarction, but contractile reserve deteriorated only in severe septal ischemia. Similarly, diastolic function was maintained in mild septal ischemia, but impaired in severe septal ischemia. We concluded that RV systolic and diastolic functions are closely related to interventricular septal ischemia.     

Ultrasonic tissue characterization of acute canine myocardial infarction

This study assessed changes in left ventricular texture on two-dimensional (2-D) echocardiography after experimental myocardial infarction. In 13 dogs, the left anterior descending coronary artery (LAD) was occluded for 3 h, followed by 1 h of reperfusion and sacrifice. Two-dimensional echocardiography was performed pre-LAD occlusion, 3 h post occlusion and 1 h after reperfusion by placing a 5 MHz transducer on the chest wall. After sacrifice, triphenyltetrazolium chloride staining was performed on 1 cm thick left ventricular cross-sectional slices. Five dogs served as controls (shams). Two-dimensional echocardiograms were digitized and in the region of left ventricular asynergy (area of myocardial infarction), and adjacent normal area, the mean pixel intensities (+/- SD) were calculated. There was no significant change in the mean pixel intensity from 0 through 4 h in the lateral (22.8 +/- 1.3 and 23.4 +/- 1.8) and anteroseptal (23.2 +/- 1.9 and 22.6 +/- 1.9) regions in sham operated dogs. In dogs undergoing LAD occlusion, the mean pixel intensity from the pre- to post occlusion period showed no significant change in the lateral (normal) area, 24.4 +/- 2.7 versus 24.7 +/- 2.9. In the area of wall motion abnormality (area of myocardial infarction) the mean pixel intensity increased from 25.4 +/- 2.7 to 33.7 +/- 4.5, P less than 0.01. There was no significant change in the mean pixel intensity between the 3 h post occlusion and post reperfusion period in either the lateral (normal) or anteroseptal areas of the left ventricle. The area of left ventricular asynergy corresponded to the area of myocardial infarction on triphenyltetrazolium chloride stain.(ABSTRACT TRUNCATED AT 250 WORDS)     

Noninvasive assessment of left and right ventricular filling in myocardial infarction with a two-dimensional Doppler echocardiographic method

Inflow characteristics of left and right ventricular filling were assessed in 40 patients with myocardial infarction and in 10 normal subjects by pulsed Doppler echocardiography. Patients with myocardial infarction were subdivided into four groups, focusing on the involvement of right ventricular and septal branches of the coronary arteries. Group I consisted of 11 patients with anterior infarction who showed an obstructive lesion of the proximal left anterior descending branch involving the first septal perforator with a patent right coronary artery. Group II consisted of 10 patients with inferior infarction who showed an obstructive lesion of the proximal right coronary artery involving the right ventricular branch. Group III consisted of 12 patients with both anterior and inferior infarction who showed obstructive lesions of both the proximal left anterior descending branch and the right coronary artery involving the right ventricular branch. Group IV consisted of seven patients with lateral infarction who showed an obstructive lesion of the diagonal branch or branches of the circumflex coronary artery with a patent left anterior descending branch and right coronary artery. Three measurements were performed from the transmitral and transtricuspidal inflow velocity patterns to assess the left and right ventricular diastolic behaviors. These measurements were: acceleration half-time, deceleration half-time of early diastolic rapid inflow, and the ratio of the peak velocity of early diastolic rapid inflow to that of the late diastolic inflow due to the atrial contraction. Impaired diastolic filling of the left ventricle compensated by enhanced left atrial contraction was observed in patients with myocardial infarction from groups I, II, III and IV.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative significance in systolic ventricular interaction.

STUDY OBJECTIVE--The aim was to measure the systolic coupling between the ventricles and to determine the relative importance of ventricular interaction in the pressure development of each ventricle. DESIGN--Acute studies were done in dogs to measure the changes in right and left ventricular pressures (dPr, dPl) caused by sudden changes in left ventricular pressure (dPl') with release of an aortic constriction, and sudden changes in right ventricular pressure (dPr') with release of a pulmonary artery constriction, respectively. The instantaneous cross talk gain [dPr/dPl' (Klr) or dPl/dPr' (Krl)] was calculated during the ejection phase. The potential systolic pressure generated by the contralateral ventricle was evaluated as the cross talk gain multiplied by the contralateral systolic developed pressure. EXPERIMENTAL MATERIAL--Studies were done in eight random source dogs (12-18 kg), anaesthetised with sodium pentobarbitone. MEASUREMENTS AND MAIN RESULTS--The maximal Klr was lower than the maximal Krl, at 0.09 (SD 0.05) v 0.25 (0.06), and the mean Klr also was lower than the mean Krl, at 0.04 (0.02) v 0.10 (0.03), p less than 0.05. The potential right ventricular pressures developed by the left ventricle [maximum 10.3(5.6), mean 4.8(2.7) mm Hg] were not significantly different from the potential left ventricular pressures developed by the right ventricle [maximum 8.8(2.7), mean 3.4(0.7) mm Hg]. However, the ratio between the potential transmitted pressure and the measured developed pressure was greater in the right ventricle [maximum 39.0(21.1), mean 17.8(8.9)%] than in the left ventricle [maximum 11.1(7.1)%, p less than 0.05; mean 3.9(1.5)%, p less than 0.01]. This suggests that about 20-40% of the right ventricular systolic pressure may result from the left ventricle and about 4-10% of the left ventricular systolic pressure may result from right ventricle. CONCLUSIONS--Although the pressure coupling was greater in right to left ventricular interaction, right ventricular pressure generation may be more dependent on the left ventricle. Systolic ventricular interaction may be more important for right ventricular systolic function. Further, the parameters of right ventricular systolic function currently used may be considerably affected by the left ventricle.