6692065
Right ventricular infarction causes heterogeneous autonomic denervation of the viable peri-infarct area.
BACKGROUND
Because efferent autonomic pathways to the right ventricle (RV) differ from the efferent autonomic projections to the left ventricle (LV), we assessed the effects of RV infarction on this innervation.


METHODS AND RESULTS
We measured the ventricular effective refractory period (ERP) shortening in response to bilateral ansae subclaviae stimulation and ERP lengthening induced by bilateral vagal stimulation as markers of autonomic innervation before and after RV myocardial infarction (RVMI) produced by coronary ligation (n=28 dogs) or intracoronary latex injection (n=18 dogs) into a marginal branch of the right coronary artery in open-chest anesthetized dogs. In each dog, ERPs measured in viable peri-infarct area at two RV outflow tract (RVOT) sites and two septal and four lateral sites at the RV free wall after RVMI showed reduced or absent ERP shortening during bilateral ansae subclaviae stimulation laterally, septally, and at RVOT sites 3 hours after RVMI. ERP shortening in response to infused norepinephrine was still present. Bilateral vagal stimulation during background norepinephrine infusion (0.10 to 0.25 microg/kg per minute) lengthened the ERP at all test sites before latex injection. After transmural RVMI, vagally induced ERP prolongation was attenuated or lost at lateral, septal, and RVOT test sites.


CONCLUSIONS
RVMI causes sympathetic and vagal denervation at viable sites at the RVOT, lateral, and, to a lesser extent, septal sides of the viable peri-infarct area. Autonomic denervation in the RVOT might contribute to the development of ventricular tachyarrhythmias after the acute stage of myocardial infarction involving the RV.
35287982
Nondominant right coronary artery occlusion presenting with isolated right ventricular infarction and ventricular fibrillation.
It is generally believed that serious complications are unlikely in a myocardial infarction resulting from occlusion of a nondominant right coronary artery. A case of isolated right ventricular infarction caused by total occlusion of a nondominant right coronary artery complicated by two episodes of ventricular fibrillation is presented.
25131066
Right ventricular infarction: identification by hemodynamic measurements before and after volume loading and correlation with noninvasive techniques.
To evaluate the potential occurrence of right ventricular infarction, 53 patients with acute inferior transmural myocardial infarction were studied within 36 hours of symptoms by right heart catheterization, equilibrium radionuclide angiography and two-dimensional echocardiography. Technetium-99m pyrophosphate myocardial scintigraphy was performed 3 days after the onset of symptoms. The hemodynamic standard for right ventricular infarction was defined as both a right atrial pressure of 10 mm Hg or more and a right atrial/pulmonary artery wedge pressure ratio of 0.8 or more. Eight (15%) of the 53 patients had hemodynamic measurements at rest characteristic of right ventricular infarction, and 6 (11%) additional patients met these criteria after volume loading (p less than 0.05). Nineteen (37%) of the 51 patients who had radionuclide angiography had right ventricular dysfunction manifested by both a reduced right ventricular ejection fraction (less than 40%) and right ventricular regional wall motion abnormalities (akinesia or dyskinesia). An abnormal radionuclide angiogram was observed in 12 of 13 patients with hemodynamic measurements indicating right ventricular infarction. In 12 patients with an abnormal radionuclide angiographic study, right ventricular ejection fraction improved 6 to 12 weeks after infarction (27 +/- 7 to 36 +/- 9%, p less than 0.01). Twenty-two (49%) of the 45 patients with adequate two-dimensional echocardiograms had a right ventricular regional wall motion abnormality. An abnormal two-dimensional echocardiogram was seen in 9 of 11 patients with hemodynamic measurements characteristic of right ventricular infarction. Technetium-99m pyrophosphate scintigraphy was positive for right ventricular infarction in 3 of 12 patients who had hemodynamic measurements indicating right ventricular infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
12259382
Right ventricular involvement with acute inferior wall myocardial infarction identifies high risk of developing atrioventricular nodal conduction disturbances.
In 67 consecutive patients with inferior wall acute myocardial infarction (AMI), 99m-technetium pyrophosphate scintigraphy was performed 36 to 72 hours after the onset of chest pain to detect right ventricular (RV) involvement. All patients were continuously monitored during at least 3 days to detect rhythm and conduction disturbances. In 29 patients RV involvement was diagnosed by scintigraphy. None of these 29 patients showed clinical signs of right-sided heart failure. Fourteen of the 19 patients showing atrioventricular (AV) nodal condution disturbances in the setting of inferior AMI also had RV involvement. Therefore, the incidence of high-degree AV nodal block in patients with RV involvement (14 of 29 patients) was 48% compared to only 13% (5 of 38) in patients with inferior AMI without RV involvement.
25722236
Prevalence of right ventricular involvement in inferior wall infarction assessed with myocardial imaging with thallium-201 and technetium-99m pyrophosphate.
To assess the prevalence and clinical relevance of right ventricular involvement in acute inferior wall infarction, 78 consecutive patients with the latter condition were studied with thallium-201 and technethium-99m pyrophosphate myocardial imaging. Right ventricular involvement was determined from superimposition of the 45 degree left anterior oblique thallium-201 and technetium-99m pyrophosphate images. All 78 patients shoed thallium-201 defects. Sixty-four patients had positive pyrophosphate scans, and 24 of these (37.5 percent) showed right ventricular involvement. None of the patients with right ventricular involvement in this consecutive series showed the classic signs of severe right ventricular failure, although subclinicalright ventricular dysfunction may have been present. There was no significant difference in the incidence of cardiogenic shock between the groups with and without right ventricular involvement. It is concluded that right ventricular involvement in acute inferior wall infarction is relatively frequent but not necessarily associated with severe right-sided pump failure. In patients with acute inferior wall infarction and severe pump failure, dual imaging provides a simple nonivasive method of identifying the subgroup of patients with right ventricular involvement who may benefit from volume loading.
10459427
Efferent Sympathetic and Vagal Innervation of the Canine Right Ventricle
BackgroundThe functional pathways of efferent sympathetic and vagal innervation to the right ventricle (RV) might be important in a variety of disease states that involve the RV wall. The purpose of this study was to investigate those pathways. Methods and ResultsWe determined the effects of phenol and endocardial radiofrequency ablation applied to the RV anterolateral wall and outflow tract on effective refractory period (ERP) shortening during bilateral ansae subclaviae stimulation and ERP lengthening during bilateral vagal stimulation. We found that efferent sympathetic axons to the RV are located in the superficial subepicardium and that lateral sites receive sympathetic innervation predominantly from the lateral margin of the RV near the AV groove. Medial sites close to the left anterior descending coronary artery (LAD) receive sympathetic innervation from both the right lateral atrioventricular (AV) groove and regions near the LAD. At the RV outflow tract, some sympathetic fibers are located intramurally. Efferent vagal fibers are located at the RV surface within 10 mm of the right lateral AV groove; they penetrate intramurally and reach to the medial sites of the RV anterior wall. Other vagal fibers originate near the LAD and are intramural. Vagal fibers to the RV outflow tract are located intramurally either from the lateral side (close to the right coronary artery) or medial side (close to the LAD). ConclusionsEfferent vagal and sympathetic innervation of the right ventricle resembles that of the left ventricle. A major difference is that efferent sympathetic fibers to the right ventricular outflow tract are located not only in the subepicardium but in the subendocardium as well.
535901
Transmural Myocardial Infarction in the Dog Produces Sympathectomy in Noninfarcted Myocardium
Because sympathetic fibers travel in the subepicardium and generally follow the coronary arteries in a basal to apical course, we tested the hypothesis that transmural myocardial infarction that involves this subepicardial region interrupts sympathetic axons traveling through the infarct and produces sympathetic denervation at noninfarcted sites apical to the infarction. A rapidly hardening vinyl latex solution injected into the first diagonal branch of the left anterior descending coronary artery produced the transmural myocardial infarction by embolizing the vasculature. Ten dogs were studied 90 minutes after coronary artery embolization (acute) and 12 dogs were studied 7–21 days after infarction (chronic). The integrity of the sympathetic innervation was tested in an open-chest preparation of the acutely and chronically infarcted dogs by measuring endocardial and epicardial effective refractory period changes during left and right stellate stimulation. Additionally, regional myocardial norepinephrine content and fluorescence were examined in the chronically infarcted dogs. Transmural infarction was verified using nitroblue tetrazolium staining. In the 10 acutely infarcted dogs, left and right stellate stimulation shortened the effective refractory period at all 56 sites examined before infarction and at 30 sites basal or lateral to the infarction after embolization. Twenty-six noninfarcted sites apical to, but not within, the zone of infarction did not respond to left or right stellate stimulation after infarction. In the 12 chronically infarcted dogs, left and right stellate stimulation shortened the effective refractory period at all 20 sites basal to infarction. In noninfarcted sites apical to the infarction, left stellate stimulation did not shorten the eifective refractory period at 23 of 41 sites, while right stellate stimulation was ineffective at 24 of 41 sites. Both left and right stellate stimulation were ineffective at 18 of 41 sites. Twelve of 41 sites apical to the infarct had normal effective refractory period shortening during left and right stellate stimulation. In both groups of dogs, norepinephrine infusion, 0.05, ug/kg/min, i.v., shortened the refractory period at all sites apical to the infarct that did not shorten refractory period in response to stellate stimulation. In chronically infarcted dogs, myocardial norepinephrine content was reduced at the denervated sites, and histologically reduced norepinephrine fluorescence in noninfarcted, denervated myocardium was found. We conclude that transmural myocardial infarction produces heterogeneous sympathetic denervation in noninfarcted sites apical to the area of necrosis. This denervation is probably the result of interrupting sympathetic nerves coursing from base to apex.
8958452
Time Course of Denervation of Efferent Sympathetic and Vagal Nerves After Occlusion of the Coronary Artery in the Canine Heart
To determine the time course of efferent sympathetic denervation after transmural myocardial infarction (TMI) and of efferent vagal denervation after transmural or nontransmural myocardial infarction (NTMI), we measured effective refractory periods (ERP) basal and apical to TMI or NTMI in secobarbital-anesthetized, open-chest dogs. In eight dogs with latex-induced TMI, bilateral ansae subclaviae stimulation shortened ERP at all 45 apical and basal test sites before latex injection. After latex injection, ERP shortening was unchanged at all 15 basal sites but was eliminated (±2 msec shortening) at three apical sites in 5-20 minutes and at 14 of 30 apical sites 30-180 minutes after latex injection. At the remaining 13 apical sites, ERP shortening was not eliminated but attenuated significantly in 5-180 minutes. ERP shortening induced by infused norepinephrine (0.20−0.25 μg/kg/min) did not differ between basal and apical test sites 3-4 hours after latex injection; that is, no supersensitivity occurred. Of six dogs with TMI produced by ligation of multiple coronary arteries without latex injection, ERP shortening induced by efferent sympathetic neural stimulation was eliminated at 10 apical sites in four dogs over a period of 3 hours. At 14 apical sites that did not show denervation in these six dogs, ERP shortening was unchanged. In seven dogs with latex-induced TMI, bilateral vagal stimulation lengthened ERP at all 40 apical and basal test sites before latex injection. Vagally induced ERP lengthening was unchanged at all 13 basal sites after latex injection. ERP lengthening was eliminated (±1 msec lengthening) at four of 27 apical sites in 5-20 minutes and at 13 apical sites 30-180 minutes after latex injection. At the remaining 10 apical sites, ERP lengthening was not eliminated but decreased significantly 3 hours after latex injection. Of nine dogs with ligation-induced NTMI, five dogs showed elimination of vagally induced ERP lengthening at eight apical sites in 3 hours after ligation. ERP lengthening induced by vagal stimulation was unchanged at all 17 basal sites in nine dogs with NTMI. We conclude that TMI produced by latex injection and ligation of multiple coronary arteries produces heterogeneous loss of efferent sympathetic innervation in noninfarcted apical sites as early as 5-20 minutes after coronary occlusion with more complete denervation occurring over time. Loss of efferent vagal innervation also occurs heterogeneously in 5-20 minutes after coronary occlusion by latex injection (TMI) and by ligation of a diagonal branch (NTMI) and continues with more sites losing efferent responsiveness over time.
1785893
Influence of Myocardial Ischemia and Infarction on Autonomic Innervation of Heart
T he vagus and sympathetic nerves link the heart to the central nervous system, carrying information from the heart over neural afferents and to the heart over neural efferents. Although it is generally well accepted that the autonomic nervous system can promote, precipitate, or prevent the development of cardiac arrhythmias, the mechanisms by which this transpires are incompletely understood. Several excellent recent reviews provide an overall discussion of the role of the autonomic nervous system and the genesis of cardiac arrhythmias.12 This review will focus on selected recent observations concerning autonomic innervation of the heart, the effects of myocardial ischemia and infarction on such innervation, and how some of these changes can modulate the development of cardiac arrhythmias.
8175503
Protection Against Autonomic Denervation Following Acute Myocardial Infarction by Preconditioning Ischemia
To examine the effects of ischemic preconditioning on efferent autonomic responses following acute transmural myocardial ischemia/infarction (MI), the time course and extent of efferent sympathetic and vagal denervation were compared between control dogs that received a one-stage sustained coronary occlusion and preconditioned dogs that received four 5-minute coronary occlusions separated by 5 minutes of reperfusion before sustained occlusion. Effective refractory periods (ERP) basal and apical to MI were determined in the baseline state and during neural stimulation before and after preconditioning occlusions and 20, 60, 120, and 180 minutes after sustained occlusion by ligature ligation of diagonal branches of the left anterior descending coronary artery. In 10 control dogs with transmural MI, ERP shortening induced by bilateral ansae subclaviae stimulation (4-msec pulses, 2-4 Hz and 2-4 mA) was unchanged at basal sites but was attenuated at apical sites. Four of 40 apical test sites exhibited efferent sympathetic denervation (±2 msec shortening) 20 minutes after sustained occlusion. Thirteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, ERP shortening at apical sites was unchanged after preconditioning occlusions and during the first 60 minutes of sustained ischemia but was attenuated at 120 minutes. Three of 40 apical test sites became denervated during a 3-hour period. The cumulative percentage of denervated apical test sites was significantly less in the preconditioned group compared with the control group (p=0.006) despite a comparable degree of subepicardial involvement in the MI (8.2±1.0percent; vs. 8.4±1.4percent;, the ratio to the left ventricular circumference, mean±SEM). In 11 control dogs tested for efferent vagal response after MI, ERP prolongation induced by bilateral vagal stimulation (4-msec pulses, 20 Hz with current strength 0.05 mA greater than that required to produce asystole) was unchanged at basal sites, but was attenuated at apical sites, and five of 44 test sites exhibited denervation (±1 msec prolongation) 20 minutes after sustained coronary occlusion. Fourteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, vagally induced ERP prolongation was unchanged both at basal and apical sites, and none of 36 apical test sites exhibited denervation after preconditioning and during a 3-hour period of sustained coronary occlusion (p<0.001 vs. control group) despite a comparable degree of subendocardial involvement in the MI (11.8±0.8percent; vs. 11.9±1.3percent;). In preconditioned hearts, the blood flow reduction to the ischemic myocardium measured by radioactive microspheres during sustained coronary occlusion was comparable with that during the first preconditioning occlusion, indicating that an increase in collateral blood flow during MI cannot explain the protective effects of preconditioning. We conclude that preconditioning with brief episodes of ischemia preserves efferent sympathetic and vagal responses during the early period after coronary artery occlusion in the dog by mechanisms still to be determined.
15716189
Defibrillating Shocks Delivered to the Heart Impair Efferent Sympathetic Responsiveness
BackgroundFunctional studies indicate that sympathetic efferents are located in the superficial subepicardium and vagal efferents are located in the subendocardium. It is possible that electrical shocks applied directly to the heart might affect the function of these autonomic nerves. Methods and ResultsLow- (<1 J), medium- (6 to 16 J), or high- (30 to 35 J) energy truncated monophasic exponential shocks, synchronized to the R wave during sinus rhythm, were delivered over implantable patches sutured inside the pericardium in anesthetized open-chest dogs. Shortening of ventricular effective refractory period (ERP), produced by bilateral ansae subclaviae stimulation (SS), was measured before and after shock delivery. High-energy shocks shifted the SS frequency-ERP response curves downward and to the right (P<.001) for sites beneath and apical to the patches; ERP shortening at basal sites remained unchanged. Such sympathetic attenuation occurred with shocks >10 J but not with shocks <10 J, was noted 15 minutes after the shock, and showed incomplete return to control values at 3 hours. Neither low- nor high-energy shocks affected norepinephrine dose-ERP response curves, indicating normal myocardial responsiveness. Low- and high-energy shocks did not attenuate bilateral cervical vagal stimulation-induced ERP prolongation. High-energy shocks delivered over patches sutured to the outside of the pericardium showed no effects on sympathetic response, suggesting a protective effect of the pericardium against shock-induced sympathetic attenuation. ConclusionsDC shocks >10 J delivered directly to the epicardium attenuated efferent sympathetic neural function. Such changes may affect electrophysiological, as well as hemodynamic, responses to sympathetic neural stimulation after cardioversion-defibrillation.
24385021
Value of two-dimensional echocardiography, electrocardiography, and clinical signs in detecting right ventricular infarction.
Noninvasive tests for the diagnosis of right ventricular (RV) infarction--two-dimensional echocardiography (2DE), ST elevation in V4R, and clinical parameters--were compared with equilibrium gated blood pool study (GBPS) in 50 patients after acute inferior myocardial infarction. Twenty-two of 50 patients had RV wall motion abnormalities on GBPS and 20 of 50 on 2DE. Sensitivity and specificity of 2DE was 82% and 93%, ST elevation in V4R was 50% and 71%, elevation of venous pressure was 77% and 85%, and a positive Kussmaul's sign was found in 59% and 89% for the detection of RV infarction compared to GBPS. Patients with RV infarction had higher peak creatine kinase levels and lower left ventricular ejection fractions than patients without RV infarction. Three patients died and all had significant left ventricular damage. At 20 weeks' follow-up, two thirds of the patients had no residual RV wall motion abnormalities, and all but two patients showed some recovery.
25131066
Right ventricular infarction: identification by hemodynamic measurements before and after volume loading and correlation with noninvasive techniques.
To evaluate the potential occurrence of right ventricular infarction, 53 patients with acute inferior transmural myocardial infarction were studied within 36 hours of symptoms by right heart catheterization, equilibrium radionuclide angiography and two-dimensional echocardiography. Technetium-99m pyrophosphate myocardial scintigraphy was performed 3 days after the onset of symptoms. The hemodynamic standard for right ventricular infarction was defined as both a right atrial pressure of 10 mm Hg or more and a right atrial/pulmonary artery wedge pressure ratio of 0.8 or more. Eight (15%) of the 53 patients had hemodynamic measurements at rest characteristic of right ventricular infarction, and 6 (11%) additional patients met these criteria after volume loading (p less than 0.05). Nineteen (37%) of the 51 patients who had radionuclide angiography had right ventricular dysfunction manifested by both a reduced right ventricular ejection fraction (less than 40%) and right ventricular regional wall motion abnormalities (akinesia or dyskinesia). An abnormal radionuclide angiogram was observed in 12 of 13 patients with hemodynamic measurements indicating right ventricular infarction. In 12 patients with an abnormal radionuclide angiographic study, right ventricular ejection fraction improved 6 to 12 weeks after infarction (27 +/- 7 to 36 +/- 9%, p less than 0.01). Twenty-two (49%) of the 45 patients with adequate two-dimensional echocardiograms had a right ventricular regional wall motion abnormality. An abnormal two-dimensional echocardiogram was seen in 9 of 11 patients with hemodynamic measurements characteristic of right ventricular infarction. Technetium-99m pyrophosphate scintigraphy was positive for right ventricular infarction in 3 of 12 patients who had hemodynamic measurements indicating right ventricular infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
7864174
The Early Recognition of Right Ventricular Infarction: Diagnostic Accuracy of the Electrocardiographic V 4R Lead
The sensitivity and specificity of ST-segment elevation in the right precordial lead V4R as an early indicator of right ventricular infarction were examined in a consecutive series of 110 patients admitted for acute inferior myocardial infarction. The sensitivity was 82.7%, the specificity 76.9% and the positive predictive value 70% in 58 patients with right ventricular infarction documented by autopsy or a combination of radionuclide ventriculography and one or more of the following tests: echocardiography, technetium- 99m pyrophosphate scintigraphy and hemodynamic monitoring. The negative predictive value was 87.7%. Because of its simplicity and its high sensitivity and specificity, recording of V4R should be an intrinsic part of the early evaluation and electrocardiographic examination of acute inferior wall infarction.