Reliability of echocardiography in the diagnosis of right ventricular hypertrophy

The right ventricular (RV) wall thickness and dimension were measured by the technique of echocardiography in 62 patients. Thirty-six of these patients died, and the RV wall thickness was measured at necropsy for comparison with the echocardiographic measurements. The necropsy RV wall thickness measured 3.3 ± 0.6 mm in patients without right ventricular hypertrophy (RVH) and 5.9 ± 0.9 mm in patients with RVH (P<.01). The echocardiographic measurements of the diastolic RV wall thickness correlated well with the necropsy measurements of the RV wall thickness (r=.83). The sensitivity and specificity of the echocardiographic criteria in detecting RVH was superior to the electrocardiographic (ECG) criteria. Furthermore, the echocardiographic technique was useful in evaluating RVH in 18 patients with an abnormal ECG due to right or left bundle branch block or myocardial infarction. We conclude that echocardiography is reliable in diagnosing RVH.     

Right ventricular dilatation after left ventricular acute myocardial infarction is predictive of extremely high peri-infarctual apoptosis at postmortem examination in humans

BACKGROUND: Cardiac remodelling after acute myocardial infarction (AMI) is characterised by molecular and cellular mechanisms involving both left and right ventricles, and biventricular failure identifies patients with an extremely unfavourable prognosis. AIMS: To assess whether a link exists between increased myocardial apoptotic rates (AR) at sites of recent infarction and patterns of unfavourable cardiac remodelling, such as biventricular enlargement after left ventricular (LV) infarction. METHODS: Twelve patients with recent AMI involving the LV and not the right ventricle (RV) and with permanent infarct related artery occlusion were selected at necropsy. Gross pathological characteristics, such as LV and RV dilatation, and AR at site of infarction were assessed. Potential false positive results (DNA synthesis and RNA splicing) were excluded from the cell count. RESULTS: RV enlargement, defined as a tricuspidal ring greater than 120 mm, was found in five cases and was associated with LV dilatation. These patients showed significantly higher AR than the others. When the subjects were divided into three groups according to progressive cardiac remodelling (absence of cardiac dilatation, isolated LV dilatation, and biventricular enlargement), the last group had significantly higher ARs than the other two groups, showing that myocardiocyte apoptosis is increased in more unfavourable forms of cardiac remodelling. CONCLUSION: Patients with severely unfavourable cardiac remodelling, such as biventricular enlargement, have extremely high myocardiocyte apoptosis at necropsy, even late after LV myocardial infarction, supporting the role of myocardiocyte loss in determining post-infarction adverse remodelling.     

Clinical first myocardial infarction: coronary artery disease and old infarcts in 53 consecutive fatal cases from a coronary care unit

The frequency and size of previous unrecognized myocardial infarction in patients with first clinical diagnosed acute myocardial infarction are unknown. In this study, 53 consecutive patients with clinical first acute myocardial infarction which proved fatal were studied postmortem. All showed acute infarction (inclusion criterium). Acute coronary thrombosis was found in 51 (96%). One-, two-, and three-vessel disease diagnosed by postmortem coronary angiography (diameter stenosis greater than or equal to 75%) was present in 17 (32%), 22 (42%), and 14 (26%), respectively. One or more old infarcts were found in 24 of the cases (45%) despite no history of previous myocardial infarction. Old infarcts were found in 86% of the hearts with three-vessel disease and in 55% of the hearts with two-vessel disease, but none were found in the hearts with one-vessel disease. The median weight of the old infarcts was 4 grams (range: 0.5 to 25 grams) corresponding to 5% (0.5 to 14%) of the ventricular myocardium. Thus, two- or three-vessel coronary artery disease and old infarcts are often present in patients dying from their clinical first acute myocardial infarction.     

Cardiac ruptures in northern Norway. A retrospective study of 104 cases

In 4,649 autopsies performed, in 1972-1985, 824 cases of acute myocardial infarction were found. Of these, 104 (12.6%) had cardiac rupture. Ten cases had rupture of the interventricular septum. The clinical and pathological records were reviewed, and the rupture group was compared with a control group of 100 patients who died from acute myocardial infarction without rupture. Of the patients with rupture, 85% died during the first week after the onset of myocardial infarction; three patients with rupture died suddenly without previous clinical evidence of myocardial infarction. Rupture occurred only in hearts with transmural infarcts, and predominantly in the anteroseptal wall. Patients with rupture had significantly higher blood pressure, fewer previous infarcts, higher frequency of coronary thrombi, less myocardial scar tissue and lower heart weight compared to the control group. There were no significant differences regarding age and sex distribution, physical effort at the symptom debut or death, medication, previous and present diseases other than infarcts, complications or the degree of atherosclerosis in the coronary arteries or aorta.     

Right ventricular involvement in anterior myocardial infarction: a tissue Doppler-derived strain and strain rate study

OBJECTIVE:

Strain and strain rate imaging is currently the most popular echocardiographic technique that reveals subclinical myocardial damage. There are currently no available data on this imaging method with regard to assessing right ventricular involvement in anterior myocardial infarction. Therefore, we aimed to evaluate right ventricular regional functions using a derived strain and strain rate imaging tissue Doppler method in patients who were successfully treated for their first anterior myocardial infarction.

METHODS:

The patient group was composed of 44 patients who had experienced their first anterior myocardial infarction and had undergone successful percutaneous coronary intervention. Twenty patients were selected for the control group. The right ventricular myocardial samplings were performed in three regions: the basal, mid, and apical segments of the lateral wall. The individual myocardial velocity, strain, and strain rate values of each basal, mid, and apical segment were obtained.

RESULTS:

The right ventricular myocardial velocities of the patient group were significantly decreased with respect to all three velocities in the control group. The strain and strain rate values of the right mid and apical ventricular segments in the patient group were significantly lower than those of the control group (excluding the right ventricular basal strain and strain rate). In addition, changes in the right ventricular mean strain and strain rate values were significant.

CONCLUSION:

Right ventricular involvement following anterior myocardial infarction can be assessed using tissue Doppler based strain and strain rate     

大鼠实验性左室心肌梗塞对右室收缩性能的影响

对左室心肌梗塞(MI)是否会直接影响右室功能,至今尚有争议。本实验观察大鼠左室MI时右室dp/dt max的改变及其与左室dp/dt max和梗塞范围(IS)间的关系。结果发现冠脉结扎后1天,在左室dp/dt max显著降低的同时,右室dp/dt max也显著降低,且与左室dp/dt max呈显著的直线正相关,而与IS呈显著的直线负相关。在冠脉结扎后3天时,左室dp/dt max有显著恢复,但仍低于对照水平,而右室dp/dt max已恢复正常,且与左室的dp/dt max和IS间不再具有显著的直线相关关系。由此证明;在大鼠左室MI早期,右室收缩性能可受到直接影响,影响的程度与IS及左室收缩性能降低的程度相关;但当左室收缩性能恢复到一定程度时,这种影响消失。     

Quantitative analysis of myocardial infarction in (NZW x BXSB)F1 hybrid mice with systemic lupus erythematosus and small coronary artery disease.

Male (NZW x BXSB)F1 mice ([W x B]F1) were used as a model for small coronary artery disease. The mortality rate for 162 mice was 0% at 12 weeks and 37% at 24 weeks. The incidence of myocardial infarction (MI) was 0% at 12 weeks, 22% at 16 weeks, 39% at 20 weeks, and 53% at 24 weeks. In 29 of the 35 (W x B)F1 male mice with MI, small multiple infarctions were noted in the right ventricular free wall and anterior, lateral, posterior, and septal ventricular walls. In 25 of the 29 hearts with multiple infarcts, the infarcts in the same heart were at the same histologic stage. Twenty-one of these hearts showed only replacement fibrosis, and 4 hearts showed only granulation. The remaining 4 hearts with multiple infarcts exhibited coagulation necrosis plus fibrosis or granulation. Quantitative analysis of the infarct size revealed that in the 35 (W x B)F1 males with MI, the relative area of MI (%MI) was significantly larger in the right ventricular free wall (6.7% +/- 8.4%) than in the ventricular septum (1.9% +/- 2.4%) or in the left ventricular free wall (2.1% +/- 2.5%). The %MI was greatest in the right third (3.6% +/- 5.4%) of the ventricular septum and in the outer third (2.9% +/- 3.3%) of the left ventricular free wall. The %MI did not increase with age. In 11 of the 35 (W x B)F1 mice, 27 intramural small arteries showed marked obliterative lesions. Most of them were in the right ventricular free wall, the right third of the ventricular septum, or the outer third of the left ventricular free wall. There was no evidence of stenosis in the extracardiac major coronary arteries. In addition, the infarct showed a whirlpool-like configuration, and x-ray photographs revealed that the small intramural coronary arteries had a whirlpool-like configuration. It is concluded that in (W x B)F1 males multiple small infarcts appear at the same time due to small coronary artery disease. The whirlpool configuration of the infarct reflects the special anatomy of the intramural coronary arteries in the mice.     

Effect of a flexible ventricular restraint device on cardiac remodeling after acute myocardial infarction

The effects of a flexible ventricular restraint device on left ventricular (LV) dilatation and hypertrophy after transmural infarction are examined in an ovine model. Left ventricular remodeling and dilatation occurs after extensive myocardial infarction. A flexible ventricular restraint made from a nitinol mesh was evaluated in adult female sheep (n=14). Cardiac magnetic resonance imaging scans and hemodynamic measurements were completed before and 6 weeks after anterior myocardial infarction. Treatment animals (n=7) received passive ventricular restraint concurrently with LV infarction; the others (n=7) served as controls. Increases in LV end-diastolic volume index were significantly less in the restraint group than in controls (0.20+/-0.41 vs 0.83+/-0.50 ml/kg, p<0.03). End-systolic volumes increased less in treatment animals (0.43+/-0.28 vs 0.90+/-0.38 ml/kg, p<0.03). Control hearts showed an increase in LV mass after infraction, whereas LV mass decreased in restrained hearts (0.14+/-0.19 vs -0.25+/-0.36 g/kg, p<0.03). Hemodynamic studies showed similar changes after infarction for the control and the device group. Gross and microscopic examination showed no device-induced epicardial injury. A flexible ventricular restraint device attenuated remodeling after acute myocardial infarction in sheep.     

Catenoidal shape of the interventricular septum acquired secondary to myocardial infarction

A catenoidal, or saddle-shaped, configuration of the interventricular septum, concave toward the left ventricular cavity in the transverse plane, but convex toward the left ventricular cavity in the apex to base plane, occurs in idiopathic hypertrophic subaortic stenosis and possibly may lead to septal hypertrophy and immobility. The authors also have observed catenoidal shape of the interventricular septum in hearts with myocardial infarcts. They reviewed 1,415 hearts examined after postmortem arteriography and fixation in distention from patients autopsied at The Johns Hopkins Hospital. Among 586 hearts with myocardial infarcts, there were 54 (9%) with a catenoidal shape of the interventricular septum. The infarcts, 45 anterior septal and 9 inferior and lateral, appeared to account for the reversal of normal apex to base curvature, although coexistent idiopathic hypertrophic subaortic stenosis could not be excluded in 3 patients. There was moderate or marked infarct expansion in 25/54 (46%) and septal or free wall rupture in 8 (15%) hearts. Reduced average net septal curvature in the 54 hearts, highly significant compared with that in 80 hearts without infarcts (P less than 0.001), would reduce the septum's contribution to left ventricular function and may contribute to the observed postinfarct congestive failure, 30/54 (56%), and hypoperfusion, 7/54 (13%). The results suggest that some myocardial infarcts may produce a catenoidal shape of the interventricular septum that could reduce the functional activity of the surviving uninfarcted basilar portion of the septum and thereby contribute to postinfarction cardiac dysfunction.     

Comparison of myocardial infarction with sequential ligation of the left anterior descending artery and its diagonal branch in dogs and sheep

We report a comparison of the effects of myocardial infarction in dogs and sheep using sequential ligation of the left anterior descending artery (LAD) and its diagonal branch (DA), with hemodynamic, ultrasonographic and pathological evaluations. Five animals were used in each group. After surgical preparation, the LAD was ligated at a point approximately 40% of the distance from the apex to the base of the heart, and after one hour, the DA was ligated at the same level. Hemodynamic and ultrasonographic measurements were performed preligation, 30 minutes after LAD ligation, and 1 hour after DA ligation. As a control, two animals in each group were used for the simultaneous ligation of the LAD and the DA. Two months after the coronary ligation, the animals were evaluated as previously, and killed for postmortem examination of their hearts. All seven animals in the dog group survived the experimental procedures, while in the sheep group only animals with sequential ligation of the LAD and DA survived. Statistically significant decreases in systemic arterial blood pressure and cardiac output, and an increase in the pulmonary artery capillary wedge pressure (PACWP) were observed one hour after sequential ligation of the LAD and its DA in the sheep, while only systemic arterial pressures decreased in the dog. Ultrasonographic analyses demonstrated variable degrees of anteroseptal dyskinesia and akinesia in all sheep, but in no dogs. Data two months after coronary artery ligation showed significant increases in central venous pressure, pulmonary artery pressure, and PACWP in the sheep, but not in the dog. Left ventricular end-diastolic dimension and left ventricular end-systolic dimension in ultrasonographic studies were also increased only in the sheep. Pathologically, the well-demarcated thin-walled transmural anteroseptal infarcts with chamber enlargement were clearly seen in all specimens of sheep, and only-mild-to-moderate chamber enlargements with endocardial fibrosis were observed in the dog hearts. In conclusion, this study confirms that the dog is not a suitable model for myocardial infarction with failure by coronary artery ligation despite negligent operative mortality, when compared directly with an ovine model.     

Nuclear medical determination of left ventricular diastolic function in coronary heart disease

In 191 patients with confirmed coronary disease we determined the left ventricular diastolic function with the Nuclear Stethoscope by the aid of the Peak Filling Rate (PFR) and the Time to Peak Filling Rate (TPFR). Moreover we investigated the ejection fraction (EF). 123 patients had already suffered a myocardial infarction, of these 59 an anterior wall infarction and 64 an inferior wall infarction. The remaining 68 patients had a CAD without a history of myocardial infarction. The PFR was 2.20 +/- 0.64 EDV/sec in the 59 patients after anterior wall infarction and 2.64 +/- 0.82 EDV/sec in the 64 patients after inferior wall infarction and 2.83 +/- 0.84 EDV/sec in 68 patients with coronary artery disease without a history of myocardial infarction. The TPFR was 178 +/- 36.7 msec after anterior and 157 +/- 49.2 msec after inferior wall infarction and 156 +/- 47 msec in the patients with CAD without previous infarction. The left ventricular diastolic function (PFR and/or TPFR) was abnormal in 87% after anterior wall infarction and in 81% after inferior wall infarction. In comparison with this the ejection fraction was reduced in 66% in anterior and in 61% after inferior wall infarction at rest. These results indicate that the resting diastolic function appears to be more informative for evaluation of a left ventricular dysfunction than the systolic function at rest.     

Structural basis of ventricular arrhythmias in human myocardial infarction: A hypothesis

The present study was undertaken using light and electron microscopic techniques to determine whether Purkinje fibers survive in the subendocardial region of anteroseptal infarcts in humans. Tissue was obtained for this purpose from 11 patients with 12 documented infarctions at the time of autopsy; six patients died within 72 hours of the infarction and five had healed infarcts. Seven of the 11 patients had ventricular arrhythmias.Light microscopic study indicated that intact cells with a normal appearance remained on the subendocardial surface, although the underlying ventricular muscle either was necrotic or was replaced by fibrous tissue. Electron microscopy demonstrated that these intact surviving cells over the surface of the infarct had few randomly oriented myofibrils, abundant glycogen, and other characteristics of Purkinje fibers. These cells could be readily distinguished from normal or infarcted ventricular muscle cells. Purkinje fibers, the most peripheral part of the conduction system, survive in extensive anteroseptal infarcts and may be the site of origin of ventricular arrhythmias.     

Left and right ventricular diastolic function during acute pericardial tamponade

The aim of the study was to determine the effect of acute pericardial tamponade on left (LV) and right ventricular (RV) intracavitary and transmural pressure-volume (P-V) relations and to assess the effect of changing blood volume during tamponade on LV and RV volumes. The experiments were done in 11 acutely instrumented anaesthetized dogs in which LV and RV volumes were determined by computed tomography (CT) (n = 5) and LV and RV diameters by sonomicrometry (n = 6). Pressures were measured in the pericardium (balloon transducer), in the aorta and in the ventricles. Incremental pericardial infusion (up to 180 ml) caused a progressive left and upward shift of the LV and the RV intracavitary P-V relationship. This shift was entirely due to increased pericardial pressure (PP). The induction of tamponade caused no change in the LV and RV transmural P-V relationship. During tamponade with ventricular filling pressures above 10-15 mmHg, blood volume expansion caused only minimal increase in LV and RV volumes. In conclusion, pericardial tamponade shifted the LV and the RV intracavitary diastolic P-V relation by increasing PP. However, there was no change in the transmural P-V relationship, indicating unchanged myocardial compliance. Volume loading caused only minimal increase in LV and RV volumes during tamponade.     

Cellular response of the evolving myocardial infarction after therapeutic coronary artery reperfusion

This study describes the cellular response of the evolving myocardial infarction in humans after early coronary artery reperfusion by one or more of the following therapies: streptokinase, percutaneous transluminal coronary angioplasty, tissue plasminogen activator, and/or coronary artery bypass graft surgery. Postmortem histologic changes were compared in two groups (n = 43 pairs) of human hearts with acute myocardial infarction matched for clinical age and left ventricular location of the infarct. The treatment group received one or more of the forms of reperfusion therapy. The control group received conventional therapy. The treatment group was judged to have an older histologic age infarct, P less than 0.002, compared with documented clinical age. For example, infarcts that were clinically 4 days old or less were judged histologically to be 1 day older. The treatment group had a higher Cellular Response Index, P less than 0.017; more hemorrhage within the infarct, P less than 0.001; a greater extent of selective myocardial cell necrosis, and a lesser extent of coagulation necrosis, P less than 0.05; more patchy, nontransmural distribution of necrosis, P less than 0.04; and a more florid cellular response, specifically more macrophages, P less than 0.034, and reactive stromal cells, P less than 0.05. In infarcts less than 3 days old clinically, the treatment group had hemorrhage and a cellular response which were wide-spread throughout the lesion, P less than 0.05, n = 18 pairs. In infarcts 3 to 4 days old clinically, the treatment group had a florid cellular response due to more macrophages, P less than 0.05, n = 9 pairs. In infarcts 5 to 10 days old, the treatment group had more macrophages, P less than 0.01; and more phagocytosis, P less than 0.003. In infarcts 10 to 40 days old clinically, the treatment group had scar formation that was patchy, P less than 0.05. In conclusion, this study demonstrates that early therapeutic coronary artery reperfusion after an acute myocardial infarction alters the pattern of injury and the cellular response to the evolving myocardial infarction so that the classical criteria for infarcts need to be modified.     

Maximal oxygen consumption is best predicted by measures of cardiac size rather than function in healthy adults

Training induces changes in cardiac structure and function which improves cardiac output (CO) and oxygen delivery during exercise. It is unclear whether it is cardiac structure or function which is of greatest importance in determining maximal oxygen consumption (VO(2max)). In 55 subjects (15 non-athletes, 32 amateur and 8 elite athletes), left and right ventricular (LV and RV) volumes and mass were assessed by magnetic resonance imaging (CMR). Comprehensive traditional and novel echocardiographic measures included colour-coded Doppler echocardiography to assess myocardial velocities, strain and strain rate at rest and maximal exercise in both ventricles. Measures of cardiac size and function were assessed as univariate and multivariate predictors of VO(2max). LV and RV mass correlated strongly with VO(2max) (r = 0.79 and r = 0.65, respectively, p < 0.0001), as did LV and RV end-diastolic volumes (r = 0.68 and r = 0.75, p < 0.0001) and heart rate reserve (r = 0.60, p < 0.0001). Measures of myocardial function were not predictive of VO(2max) with the exception of RV diastolic velocities (r = 0.32 and r = 0.36 for rest and exercise, respectively, p < 0.05). On multivariate analysis, only RV end-diastolic volume, LV mass and heart rate reserve were independent predictors (beta = 0.28, 0.45 and 0.27 respectively, p < 0.0001) and together explained 73% of the variance in VO(2max). Measures of cardiac morphology are strongly associated with VO(2max) in healthy adults and well-trained athletes. A combination of ventricular volume, mass and heart rate reserve explains much of the variance in VO(2max), whilst measures of myocardial function do not further strengthen predictive models.     

The effects of asymmetric ventricular filling on left–right ventricular interaction in the normal rat heart

Heart failure is characterised by ventricular dysfunction and with the potential for changes to ventricular volumes constraining the mechanical performance of the heart. The contribution of this interaction from geometric changes rather than fibrosis or metabolic changes is unclear. Using the constant pressure Langendorff-perfused rat heart, the volume interaction between left ventricle (LV) and right ventricle (RV) was investigated. RV diastolic stiffness (P?<?0.001) and developed pressure (P?<?0.001) were significantly lower than LV. When the RV was fixed at the end-diastolic volume (EDV) or EDV?+?50?%, both LV systolic and diastolic performance were unaffected with increasing LV balloon volume. However, at fixed LV volume, RV systolic performance was significantly decreased when LV volume increased to EDV?+?50?% when RV volume was increased incrementally between 50 and 300?μl (P?<?0.001). Systolic interaction in RV was noted as declining RV peak systolic load with increasing LV systolic pressure (P?<?0.05) and diastolic interaction was noted for RV when LV volume was increased from EDV to EDV?+?50?% (P?<?0.05). RV diastolic wall stress was increased with increasing LV balloon volume (P?<?0.05), but LV wall stress was unaltered at fixed RV balloon volume. Taken together, increasing LV volume above EDV decreased systolic performance and triggered ventricular constraint in the RV but the RV itself had no effect on the performance of the LV. These results are consistent with overload of the LV impairing pulmonary perfusion by direct ventricular interaction with potential alteration to ventilation–perfusion characteristics within the lung.     

Elevated sympathetic response of epicardium proximal to healed myocardial infarction

Sympathetic nerve interaction with cardiac electrophysiology was evaluated in healed myocardial infarction by monitoring the effects of sympathetic nerve stimulation on local epicardial refractoriness in cats. Single-stage distal coronary artery ligation was used to induce myocardial infarction. Regions overlying and surrounding infarcts 3 mo after healing and comparable regions in sham-operated and normal unoperated hearts were studied. Local ventricular muscle refractory periods were measured by the extrastimulus technique from 1) the epicardium overlying the infarct, 2) the area bordering the infarct, and 3) a normal area proximal to the infarct on the anterior free wall of the left ventricle. Bilateral stimulation of the ansa subclavia induced significant and disparate refractory period shortening (P less than or equal to 0.01) in hearts with healed myocardial infarction. Shortening was greatest in the normal area [-26 +/- 8 (+/-SD) ms], less in the border area (-15 +/- 6), and least in the infarct area (-7 +/- 2). In contrast, refractory periods measured in noninfarcted hearts shortened significantly (P less than or equal to 0.01) but uniformly and to a lesser extent during sympathetic stimulation. We conclude 1) the effects of sympathetic nerve stimulation are more pronounced in the areas proximal to healed infarction than in similar areas of noninfarcted hearts and 2) a marked disparity in sympathetic responsiveness occurs in hearts with healed myocardial infarction.     

Cardiovascular pathology in renal transplant recipients

Various cardiovascular complications are among the major causes of mortality in renal transplant recipients. The authors examined the cardiovascular findings from necropsy of 18 renal transplant patients. All but three of the patients showed one or more pathological abnormalities. Five patients exhibited severe coronary arteriosclerosis with acute myocardial infarction with a history of myocardial infarction noted in four patients. In addition, one patient showed moderate and two showed mild coronary arteriosclerosis. Also prevalent were left ventricular (LV) hypertrophy (10/18), right ventricular (RV) hypertrophy (7/18), LV dilatation (4/18), RV dilatation (8/18), left atrial dilatation (3/18), and right atrial dilatation (6/18). Valvular abnormalities consisted of dilatations of mitral ring (1/18), pulmonic valve (2/18), and tricuspid valve (3/18). Pericarditis was found in two patients and aortic atherosclerosis in ten patients. Findings on routine chest roentgenograms and electrocardiograms did not always correspond with the anatomical findings noted on necropsy examination. The results demonstrate a marked increase in the incidence of various cardiac abnormalities in renal transplant recipients.     

Dynamics of the interventricular septum and ventricular free walls during regional ischaemia in open-chest dogs

The significance of ischaemia of the left ventricular (LV) and right ventricular (RV) free walls for the dynamics of the interventricular septum (IVS) and the right ventricle was examined in open-chest dogs. Left ventricular and RV ischaemia reduced stroke volume similarly, by 11.2 +/- 1.4% and 11.2 +/- 2.4%, respectively. The dynamics of myocardial segment lengths (SL), recorded in the LV and RV free walls and the IVS, differed. During LV ischaemia, end-diastolic SL (EDSL) and systolic shortening (SS) increased in the IVS, whereas SL remained unchanged in the RV free wall. During RV ischaemia, LV EDSL, and SS decreased. Interventricular septum EDSL also decreased, but this reduction was not statistically significant. During blood volume expansion, LV and RV function curves were shifted right, and/or downwards by LV ischaemia, whereas only the RV function curve was shifted downwards and to the right by RV ischaemia. Thus, ischaemia of the LV free wall induces activation of the Frank-Starling mechanism in the interventricular septum and a deterioration of right ventricular performance.     

Postmortem detection of inapparent myocardial infarction

Two methods of detecting early inapparent myocardial infarcts have been studied and their value in diagnostic practice compared.The better method proved to be the determination of the potassium to sodium ratio (ionic ratio) which falls in infarcted tissue within minutes of the onset of anoxia. The second method was nitro blue tetrazolium staining of gross sections of myocardium which revealed any infarct older than three and a half hours. As staining is dependent upon enzyme activity, the latter method is disturbed by autolysis. It was shown, on the other hand, that the ionic ratio (K(+)/Na(+)) was not affected by autolysis and was therefore well suited to forensic practice.Sixteen non-infarcted control hearts, plus the nine from cases of sudden death due to causes other than myocardial infarction, all yielded high ionic ratios (K(+)/Na(+)), average 1.4, and stained normally with tetrazolium (the normal controls). Positive control was provided by 20 histologically proven infarcts of which the ionic ratios (K(+)/Na(+)) were all low (average 0.7). Histochemical staining with tetrazolium delineated infarcted areas in each case.In a series of 29 sudden deaths, a cause of death other than myocardial infarction was found at necropsy in nine, mentioned above as normal controls. The remaining 20 hearts were not infarcted histologically, but were shown to be infarcted by examination of the ionic ratios (K(+)/Na(+)). These ratios were low (average 0.8) including three borderline ratios. Confirmatory evidence of infarction included nitro blue tetrazolium staining which revealed infarcts in 10 of the 20 cases, and clinical and necropsy observations.The ionic ratio (K(+)/Na(+)) decreases as the age of the infarct increases for at least 24 hours. Thereafter as healing proceeds, the ratio gradually reverts to normal. Thus, previous infarction and replacement fibrosis do not significantly alter the ionic ratio (K(+)/Na(+)). Nor is it changed by left ventricular hypertrophy, the presence of congestive cardiac failure, or digitalis therapy.It is suggested that macroscopic tetrazolium staining is a useful screening test for early inapparent myocardial infarcts. In cases where no infarct is delineated with that method estimation of the ionic ratio (K(+)/Na(+)) should be carried out on myocardium removed from standard areas on the anterior and posterior left ventricular walls.