Occlusion Of Left Circumflex Artery Research Articles

Effects of ischemic preconditioning and arterial collateral flow on ST-segment elevation and QRS complex prolongation in a canine model of acute coronary occlusion

Background During acute myocardial infarction, both ST elevation and QRS distortion on the initial electrocardiogram (ECG) have been correlated with poorer prognosis. Studies in dogs and humans suggest that these ECG markers provide information about myocardial protection from both collateral blood flow and ischemic preconditioning. Methods In a protocol designed to precondition the heart with ischemia, we examined both ST-segment elevation and QRS complex prolongation in lead II of the ECG in 23 mongrel dogs during the first and fourth episode of 5 minutes of left circumflex artery occlusion. Myocardial collateral flow was measured during each of these episodes by injection of radioactive microspheres 2.5 minutes into the episode of ischemia. Results During ischemia, the degree of elevation of the ST segments was reduced markedly in hearts preconditioned with ischemia and/or in hearts with the greatest amounts of collateral arterial flow. During the first episode of ischemia, the ST segments increased to a similar extent in severe and moderate ischemia, but less in hearts in which the ischemia was mild. However, marked QRS prolongation was present only in hearts with severe ischemia, and decreased when the hearts were preconditioned. In addition, large ischemic beds exhibited the most marked QRS prolongation, whereas small but even severely ischemic beds showed little or no change in QRS duration. Conclusion Both ST elevation and QRS prolongation are reduced by the presence of collateral flow and ischemic preconditioning. The QRS complex merits further study as an important marker of the degree of myocardial protection during human acute myocardial ischemia/infarction.

Usefulness of Three Posterior Chest Leads for the Detection of Posterior Wall Acute Myocardial Infarction

A significant proportion of patients with myocardial infarction are missed upon initial presentation to the emergency department. The 12-lead electrocardiogram (ECG) has a low sensitivity for the detection of acute myocardial infarction, especially if the culprit lesion is in the left circumflex artery (LCA). This study was designed to evaluate the benefit of adding 3 posterior chest leads on top of the 12-lead ECG to detect ischemia resulting from LC disease, using a model of temporary balloon occlusion to produce ischemia. We studied 53 consecutive patients who underwent clinically indicated coronary interventions. At the time of coronary angiography, the balloon was inflated to produce complete occlusion of the proximal LCA. We recorded and analyzed the changes noted on the 15-lead ECG, which included 3 posterior leads in addition to the standard 12 leads. In response to acute occlusion of the LCA, the posterior chest leads showed more ST elevation than the other leads, and more patients had ST elevation in the posterior leads than in any other lead. The 15-lead ECG was able to detect>or=0.5 mm (74% vs 38%, p<0.0001) and >or=1 mm (62% vs 34%, p<0.0001) ST elevation in any 2 contiguous leads more frequently than the 12-lead ECG. In conclusion, the 15-lead ECG identified more patients with posterior myocardial wall ischemia because of temporary balloon occlusion of the LC than the 12-lead ECG. This information may enhance the detection of posterior MI in the emergency department and potentially facilitate early institution of reperfusion therapy.

Regional and temporal heterogeneity of postsystolic wall thickening is associated with left ventricular asynchrony in normal and experimental stunned myocardium

Postsystolic wall thickening (PSWT) occurs after aortic valve closure. We investigated the influence of ischemia location and wall interactions on PSWT in normal and stunned myocardium. Twenty-two dogs were studied. Seven chronically instrumented dogs (sonomicrometry) underwent 10-min coronary artery occlusion (CAO) of left circumflex artery ("LCX stunning") and seven other dogs underwent 10-min CAO of the anterior descending artery ("LAD stunning") followed by reperfusion. At baseline, there was no PSWT in the anterior wall whereas posterior wall started and finished to thicken after the anterior wall, demonstrating PSWT. With LCX stunning, PSWT was observed in the posterior wall without affecting the remote anterior wall. With LAD stunning, PSWT in the anterior wall was transient and of lower magnitude Vs. posterior wall; in the remote posterior wall, PSWT previously observed at baseline, almost vanished. Postsystolic to systolic wall thickening ratio identified (ROC analysis) normal, ischemic and stunned myocardium with different amplitudes between walls. Tissue Doppler Imaging demonstrated similar pattern in basal, mid and apical segments (additional n = 4 for both LCX and LAD stunning). The present study demonstrates that location of ischemia and wall interactions produce discrepancies in PSWT between anterior and posterior walls in stunned myocardium.

Effects of acute ischemic mitral regurgitation on three-dimensional mitral leaflet edge geometry☆☆☆

Improved quantitative understanding of in vivo leaflet geometry in ischemic mitral regurgitation (IMR) is needed to improve reparative techniques, yet few data are available due to current imaging limitations. Using marker technology we tested the hypotheses that IMR (1) occurs chiefly during early systole; (2) affects primarily the valve region contiguous with the myocardial ischemic insult; and (3) results in systolic leaflet edge restriction. Eleven sheep had radiopaque markers sutured as five opposing pairs along the anterior (A(1)-E(1)) and posterior (A(2)-E(2)) mitral leaflet free edges from the anterior commissure (A(1)-A(2)) to the posterior commissure (E(1)-E(2)). Immediately postoperatively, biplane videofluoroscopy was used to obtain 4D marker coordinates before and during acute proximal left circumflex artery occlusion. Regional mitral orifice area (MOA) was calculated in the anterior (Ant-MOA), middle (Mid-MOA), and posterior (Post-MOA) mitral orifice segments during early systole (EarlyS), mid systole (MidS), and end systole (EndS). MOA was normalized to zero (minimum orifice opening) at baseline EndS. Tenting height was the distance of the midpoint of paired markers to the mitral annular plane at EndS. Acute ischemia increased echocardiographic MR grade (0.5+/-0.3 vs 2.3+/-0.7, p<0.01) and MOA in all regions at EarlyS, MidS, and EndS: Ant-MOA (7+/-10 vs 22+/-19 mm(2), 1+/-2 vs 18+/-16 mm(2), 0 vs 17+/-15 mm(2)); Mid-MOA (9+/-13 vs 25+/-17 mm(2), 3+/-6 vs 21+/-19 mm(2), 0 vs 25+/-17 mm(2)); and Post-MOA (8+/-10 vs 25+/-16, 2+/-4 vs 22+/-13 mm(2), 0 vs 23+/-13 mm(2)), all p<0.05. There was no change in MOA throughout systole (EarlyS vs MidS vs EndS) during baseline conditions or ischemia. Tenting height increased with ischemia near the central and the anterior commissure leaflet edges (B(1)-B(2): 7.1+/-1.8mm vs 7.9+/-1.7 mm, C(1)-C(2): 6.9+/-1.3mm vs 8.0+/-1.5mm, both p<0.05). MOA during ischemia was larger throughout systole, indicating that acute IMR in this setting is a holosystolic phenomenon. Despite discrete postero-lateral myocardial ischemia, Post-MOA was not disproportionately larger. Acute ovine IMR was associated with leaflet restriction near the central and the anterior commissure leaflet edges. This entire constellation of annular, valvular, and subvalvular ischemic alterations should be considered in the approach to mitral repair for IMR.

Conduction disturbances and paroxysmal atrial fibrillation during acute inferior myocardial infarction

Associated symptoms and conduction disturbances are reported during acute inferior myocardial infarction. Differentiation of right coronary artery from left circumflex artery occlusion may be difficult since both can present an electrocardiographic pattern of inferior myocardial infarction. Paroxysmal atrial fibrillation is considered a frequent complication of acute myocardial infarction and the patients with paroxysmal atrial fibrillation probably should be targeted for earlier and more aggressive treatment. These patients in the thrombolytic era have a better overall outcome than counterparts in the prethrombolytic era. We describe a case of conduction disturbances and paroxysmal atrial fibrillation in a 51-year-old Italian man with acute inferior myocardial infarction and right coronary artery stenosis.

Growth-hormone-releasing peptide 6 (GHRP6) prevents oxidant cytotoxicity and reduces myocardial necrosis in a model of acute myocardial infarction

Therapies aimed at enhancing cardiomyocyte survival following myocardial injury are urgently required. As GHRP6 [GH (growth hormone)-releasing peptide 6] has been shown to stimulate GH secretion and has beneficial cardiovascular effects, the aim of the present study was to determine whether GHRP6 administration reduces myocardial infarct size following acute coronary occlusion in vivo. Female Cuban Creole pigs were anaesthetized, monitored and instrumented to ensure a complete sudden left circumflex artery occlusion for 1 h, followed by a 72 h reperfusion/survival period. Animals were screened clinically before surgery and assigned randomly to receive either GHRP6 (400 microg/kg of body weight) or normal saline. Hearts were processed, and the area at risk and the infarct size were determined. CK-MB (creatine kinase MB) and CRP (C-reactive protein) levels and pathological Q-wave-affected leads were analysed and compared. Evaluation of the myocardial effect of GHRP6 also included quantitative histopathology, local IGF-I (insulin-growth factor-I) expression and oxidative stress markers. GHRP6 treatment did not have any influence on mortality during surgery associated with rhythm and conductance disturbances during ischaemia. Infarct mass and thickness were reduced by 78% and 50% respectively, by GHRP6 compared with saline (P<0.01). More than 50% of the GHRP6-treated pigs did not exhibit pathogological Q waves in any of the ECG leads. Quantitative histopathology and CK-MB and CRP serum levels confirmed the reduction in GHRP6-mediated necrosis (all P<0.05). Levels of oxidative stress markers suggested that GHRP6 prevented myocardial injury via a decrease in reactive oxygen species and by the preservation of antioxidant defence systems (all P<0.05). Myocardial IGF-I transcription was not amplified by GHRP6 treatment compared with the increase induced by the ischaemic episode in relation to expression in intact hearts (P<0.01). In conclusion, GHRP6 exhibits antioxidant effects which may partially contribute to reduce myocardial ischaemic damage.

Value of ST‐segment depression in lead V4R in predicting proximal against distal left circumflex artery occlusion in acute inferoposterior myocardial infarction

Lead V(4R) faces the right ventricular free wall; it also reflects ischemia in the posterolateral wall lying opposite and manifests as ST-segment depression. The aim of this study was to evaluate the usefulness of V(4R) ST-segment depression in distinguishing proximal from distal left circumflex artery occlusion in acute inferoposterior wall myocardial infarction. We retrospectively analyzed 239 patients who had first acute inferoposterior myocardial infarction, were admitted within 6 h from onset of symptom, and had coronary angiography performed within 4 weeks. Patients who had bundle-branch block or concomitant significant stenoses in the proximal and distal segments of the same vessel or of both vessels were excluded. The electrocardiographic and angiographic findings were reviewed by two independent groups of investigators. V(4R) ST-segment depression > or =1.0 mm was found in 8 of 46 patients (17.4%) with left circumflex artery occlusion but none (0%) with right coronary artery occlusion. Among the group with left circumflex artery occlusion, the mean magnitude of V(4R) ST-segment depression was greater in proximal than distal occlusion (0.82 +/- 0.65 vs. 0.03 +/- 0.12 mm, p < 0.0001). V(4R)ST-segment depression > or =1.0 mm was found in 8 of 14 patients (57.1%) with proximal occlusion but none (0%) in 32 patients with distal occlusion. The sensitivity and specificity to predict proximal occlusion were 57.1 and 100%, respectively. V(4R) ST-segment depression > or =1.0 mm was not useful for differentiating left circumflex and right coronary artery occlusion because of its low sensitivity. It is a fairly sensitive and very specific sign of proximal left circumflex artery occlusion.

Endothelial NOS is Upregulated in the Heart During the Second Window of Protection

The role of eNOS in the heart during the second window of protection (SWOP) is a matter of debate. Fourteen dogs were chronically instrumented to measure aortic pressure, left ventricular dP/dt max, coronary blood flow, and wall thickening. In half the animals, preconditioning was induced by 10-min occlusion of left circumflex (CX) artery. Following 24 hr of reperfusion (during SWOP), hearts were excised. Western blot analysis was used to assess eNOS level in the myocardium. Coronary microvessels were obtained from CX bed and incubated in presence of endothelium-dependent agonists [carbachol (10 −8–10−5M) and bradykinin (10−5M)]; calcium ionophore A23187 (10−5M). Nitrite (NT), a metabolite of NO, was measured spectrophotometrically. Findings during SWOP were compared to those in normal hearts. The level of eNOS protein was 3-fold higher in SWOP group. Under baseline (no agonist present), NT production by coronary microvessels from SWOP group was 30% higher than that from Normal group. NT production in response to agonists was enhanced in coronary microvessels from SWOP group. These enhanced responses were abolished by L-NAME. The present findings provide evidence for an upregulation of eNOS leading to increased NO production during SWOP. This NO would be expected to provide protection to the endothelium, as well as to the surrounding myocytes, during ischemia-reperfusion.

Comparison of developmental endothelial locus-1 angiogenic factor with vascular endothelial growth factor in a porcine model of cardiac ischemia

Background This study compared the angiogenic effects of developmental endothelial locus-1 (DEL-1), vascular endothelial growth factor (VEGF), as well as the negative control, β-galactosidase (β-gal), in a porcine model of cardiac ischemia. Methods Twenty pigs underwent left circumflex artery occlusions. After 3 weeks, the animals received myocardial injections of adenovirus expressing β-gal (n=6), DEL-1 (n=7), or VEGF (n=7). At 7 weeks, animals were assessed for both function and coronary flow and compared with baseline measurements. Results Regional wall motion index and global ejection fraction showed deterioration in function in the β-gal group and no change in the VEGF and DEL-1 groups between the treatment and harvest time points. Preload recruitable stroke work suggested functional improvement in the VEGF group (35.8 ± 8.6 vs 56.4 ± 17.8, p = 0.033). The increase in the DEL-1 group was not statistically significant (27.3 ± 9.8 vs, 40.2 ± 19.4, p = 0.067). The β-gal group exhibited minimal change (30.7 ± 14.8 vs 35.9 ± 12.1, p = 0.96). Regional blood flow as assessed by fluorescent microspheres was improved under stress conditions in the VEGF group (1.00 ± 0.15 vs 1.15 ±0.22, p = 0.03). Conclusions Treatment with VEGF led to a modest improvement in regional blood flow and cardiac function in previously ischemic myocardial tissue.

Acute myocardial infarction due to occlusion of the dominant left circumflex artery proximally

Acute myocardial infarction due to occlusion of the dominant left circumflex artery proximally

Clinical Features and Outcome of Patients with Direct Percutaneous Coronary Intervention for Acute Myocardial Infarction Resulting from Left Circumflex Artery Occlusion

Little is known about the clinical features and outcome of patients with left circumflex artery (LCX) infarct-related acute myocardial infarction (AMI). This study was conducted to investigate the clinical features and outcome of patients who underwent direct percutaneous coronary intervention (d-PCI) for AMI caused by LCX occlusion, and to discover prognostic determinants in this clinical setting. Between May 1993 and October 2000, a total of 819 patients with AMI underwent d-PCI in our hospital. Sixty-seven patients (8.2%) who had LCX infarct-related AMI constituted the population of this study. Ten of 67 patients (14.9%) were in cardiogenic shock. Angiographic findings demonstrated that the incidences of triple-vessel disease, reference lumen diameter (RLD) of the LCX > or = 4.0 mm, and LCX as the dominant artery in these patients were 26.9%, 22.4%, and 34.3%, respectively. Sixteen patients (23.9%) had unsuccessful reperfusion (defined as Thrombolysis in Myocardial Infarction flow < or = 2). Univariate analysis showed that dominant LCX, RLD of the LCX > or = 4.0 mm, cardiogenic shock, precordial ST-segment depression, and complete atrioventricular block were significantly related to unsuccessful reperfusion. Multiple stepwise logistic regression analysis demonstrated that dominant LCX and cardiogenic shock were significant independent predictors of unsuccessful reperfusion. The 30-day mortality rate in the 67 patients was 14.9%. Univariate analysis demonstrated that triple-vessel disease, dominant LCX, cardiogenic shock, poor left ventricular ejection fraction, and unsuccessful reperfusion were significantly associated with 30-day mortality. By multiple stepwise logistic regression analysis, dominant LCX, cardiogenic shock, and triple-vessel disease were significant independent predictors of increased 30-day mortality. LCX infarct-related AMI has its unique clinical features. The presence of dominant LCX and cardiogenic shock were independent determinants of unsuccessful reperfusion, and the presence of dominant LCX, cardiogenic shock, and triple-vessel disease were independent determinants of increased 30-day mortality in this clinical setting.

Basic Fibroblast Growth Factor Is Upregulated in Hibernating Myocardium

Background. Ischemia is known to be a potent stimulus for the upregulation of angiogenic growth factors, such as basic fibroblast growth factor (bFGF). While previous investigations have shown that many angiogenic growth factors are upregulated in animal models of myocardial ischemia, the models used are limited in their ability to produce stable ischemia beyond a few weeks. Our laboratory uses a stable model of hibernating myocardium where later time points may be examined. Therefore, the goal of this study was to examine bFGF protein levels in the myocardium at baseline and 3 or 6 months following the onset of myocardial ischemia. Methods. A total of 18 miniswine were studied. Basal endogenous levels of bFGF were measured in control animals (n = 6) immediately following sacrifice, while 12 other pigs underwent a 90% left circumflex artery occlusion with documented hibernating myocardium by positron emission tomography (13N-ammonia) and dobutamine stress echocardiography. These animals were studied at 3 (n = 7) and 6 months (n = 5) postoperatively. At sacrifice, six 3 × 3 mm samples were harvested from the left circumflex (hibernating) myocardium. Basic FGF levels (picograms per microgram of protein) were determined using ELISA kits. Results. Basic FGF protein levels 3 months after the creation of hibernating myocardium were three times greater than in nonischemic control animals (P < 0.05), while levels at 6 months were increased sixfold compared to control animals (P < 0.05 versus both control and 3-month groups). Conclusions. Endogenous bFGF production is upregulated at 3 and 6 months in hibernating porcine myocardium. The angiogenic effects of exogenous bFGF delivered into ischemic myocardium with varying levels of endogenous growth factors must be determined.

Basic Fibroblast Growth Factor Is Upregulated in Hibernating Myocardium

Background. Ischemia is known to be a potent stimulus for the upregulation of angiogenic growth factors, such as basic fibroblast growth factor (bFGF). While previous investigations have shown that many angiogenic growth factors are upregulated in animal models of myocardial ischemia, the models used are limited in their ability to produce stable ischemia beyond a few weeks. Our laboratory uses a stable model of hibernating myocardium where later time points may be examined. Therefore, the goal of this study was to examine bFGF protein levels in the myocardium at baseline and 3 or 6 months following the onset of myocardial ischemia. Methods. A total of 18 miniswine were studied. Basal endogenous levels of bFGF were measured in control animals ( n = 6) immediately following sacrifice, while 12 other pigs underwent a 90% left circumflex artery occlusion with documented hibernating myocardium by positron emission tomography ( 13N-ammonia) and dobutamine stress echocardiography. These animals were studied at 3 ( n = 7) and 6 months ( n = 5) postoperatively. At sacrifice, six 3 × 3 mm samples were harvested from the left circumflex (hibernating) myocardium. Basic FGF levels (picograms per microgram of protein) were determined using ELISA kits. Results. Basic FGF protein levels 3 months after the creation of hibernating myocardium were three times greater than in nonischemic control animals ( P < 0.05), while levels at 6 months were increased sixfold compared to control animals ( P < 0.05 versus both control and 3-month groups). Conclusions. Endogenous bFGF production is upregulated at 3 and 6 months in hibernating porcine myocardium. The angiogenic effects of exogenous bFGF delivered into ischemic myocardium with varying levels of endogenous growth factors must be determined.

Impact of myocardial ischemia and reperfusion on ventricular defibrillation patterns, energy requirements, and detection of recovery.

Shocks that have defibrillated spontaneous ventricular fibrillation (VF) during acute ischemia or reperfusion may seem to have failed if VF recurs before the ECG amplifier recovers after shock. This could explain why the defibrillation threshold (DFT) for spontaneous VF appears markedly higher than for electrically induced VF. The DFT for electrically induced VF (E-DFT) was determined in 15 pigs before ischemia, followed by left anterior ascending or left circumflex artery occlusion. VF was electrically induced 20 minutes after occlusion, followed 5 minutes later by reperfusion. Whether spontaneous or electrically induced, VF during occlusion or reperfusion was treated with up to 3 shocks at 1.5xE-DFT. If all 3 shocks failed, shock strength was increased. Thirty minutes after reperfusion, the other artery was occluded and the protocol was repeated. Defibrillation was considered successful if postshock sinus/idioventricular rhythm was present for > or = 30 seconds. VF recurring within 30 seconds after the shock was considered immediate or delayed if the first postshock activation complex in a rapidly restored ECG recording was VF or sinus/idioventricular rhythm, respectively. Defibrillation efficacy at 1.5xE-DFT was significantly higher for electrically induced ischemic VF (76%) than for spontaneous VF (31%). The incidence of delayed recurrence after electrically induced nonischemic (3%) or ischemic (20%) VF was significantly lower than after spontaneous VF (75%). Mean VF recurrence time after spontaneous VF was 4.6+/-5.3 seconds. Spontaneous VF can be halted by a shock but then quickly restart before a standard ECG amplifier has recovered from postshock saturation, making it appear that the shock failed.

Increased cardiomyocyte apoptosis following ischemia and reperfusion in diet-induced hypercholesterolemia: relation to Bcl-2 and Bax proteins and caspase-3 activity.

It has been reported that apoptosis is a significant contributor to myocardial cell death as a result of reperfusion injury. However, whether the extent of cardiomyocyte apoptosis following ischemia and reperfusion varies in different pathophysiological backgrounds is still uncertain. In this study, we examined whether hypercholesterolemia increases the extent of myocardial reperfusion injury by aggravating cardiomyocyte apoptosis and the effects of hypercholesterolemia on the expression of Bcl-2 and Bax proteins and the activation of caspase-3. Twenty-eight male New Zealand white rabbits were fed standard chow (control, n = 14) or chow supplemented with 10% cholesterol (hypercholesterolemic, n = 14) for 8 wk. Anesthetized rabbits were then subjected to 30 min of left circumflex artery occlusion followed by 4 h of reperfusion. Apoptosis was identified as "DNA ladders" by gel electrophoresis and confirmed histologically using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay. The infarct size (% of risk region) was significantly greater in hypercholesterolemic rabbits than in controls (39 +/- 6 vs. 23 +/- 2%, P = 0.02). Very few TUNEL-positive cardiomyocytes could be identified in the nonischemic regions in both groups, consistent with an absence of DNA laddering. In contrast, TUNEL-positive cardiomyocytes were significantly displayed in the ischemic, nonnecrotic myocardium, and DNA ladder occurred in all animals. The percentage of TUNEL-positive cardiomyocytes in the ischemic nonnecrotic myocardium was significantly higher in hypercholesterolemic rabbits compared with controls (40 +/- 5 vs. 17 +/- 11%, P < 0.001). Western blot analysis showed that, in the nonischemic myocardium, hypercholesterolemic rabbits exhibited an approximately 50% increase in the expression of Bcl-2 (P < 0.05), but not Bax, than control rabbits. However, compared with controls, hypercholesterolemic rabbits exhibited a more pronounced decrease in the expression of Bcl-2 (42 +/- 4 vs. 26 +/- 2%, P < 0.01) and a similar extent of increase in the expression of Bax in the ischemic myocardium. Furthermore, hypercholesterolemic rabbits were associated with a markedly increased activation of caspase-3 within the ischemic myocardium compared to control rabbits. This study demonstrates that although hypercholesterolemia is associated with an increased myocardial Bcl-2/Bax ratio at baseline, it still significantly exacerbates cardiac reperfusion injury, not only by increasing the infarct size but also by increasing the extent of cardiomyocyte apoptosis.

Usefulness of ST elevation II/III ratio and ST deviation in lead I for identifying the culprit artery in inferior wall acute myocardial infarction

In a study of 92 patients presenting with inferior wall acute myocardial infarction, the infarct-related artery was the right coronary artery in 72 patients (78%) and the left circumflex artery in 20 (22%). An ST II/III ratio of 1 or an isoelectric ST in lead I are sensitive and specific markers of left circumflex artery occlusion, whereas an ST II/III ratio <1 (ST elevation in lead III >II) or ST depression in lead I are sensitive and specific markers of right coronary artery occlusion.

MRI of congenital coronary artery aneurysm.

A case is described in which a myocardial infarction in a young woman was associated with a congenital aneurysm of the left coronary artery. Coronary angiography had shown displacement and almost total occlusion of the left circumflex artery. MRI demonstrated that this was owing to an aneurysm of the left circumflex coronary artery.

Nonischemic End-Systolic Performance

Nonischemic end-systolic performance decreases during ischemia. These changes in performance are likely to be dependent on the size and site of the ischemic zone, as well as the prevailing loading conditions. This study was designed to examine the effect of regional and generalized changes in inotropy on nonischemic end-systolic performance, independent of the ischemic zone size. Twenty dogs were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure-thickness relationship data were obained during vena-caval balloon inflation. Measurements were obtained before and 90 s after left circumflex (LC) artery occlusion. Then, simultaneous with the occlusion of the LC artery, isoproterenol (0.04 μg/ml) was infused into the left anterior descending artery. After recovery, the same protocol was repeated before and after propranolol (0.5 mg/kg). In a separate set of animals, the same measurements were made following 2.5 and 5 μg/kg/min dobutamine. The effect of ischemia on the nonischemic end-systolic pressure-thickness relationship was expressed as the extent to which the relationship is shifted to the left. Infusion of intracoronary isoproterenol into the perfusion bed of the nonischemic zone produced a significant increase in the slope of the end-systolic pressure-thickness relationship. During ischemia, however, the extent of leftward shift of this relationship was less than that following β-blockade. Intravenous dobutamine resulted in a dose-dependent increase in the slope of the nonischemic end-systolic pressure thickness relationship, but the extent of leftward displacement of the relationship in response to regional ischemia was less than that following the control occlusion. The nonischemic segment is coupled with the nonfunctioning ischemic zone in such a way that it is required of the nonischemic segment to operate at decreased end-systolic thickness for any end-systolic pressure, the extent of which is to be determined, in part, by the size of the ischemic zone and the contractile state of the nonischemic myocardium. The lower the contractile state prior to coronary occlusion the greater extent of leftward shift of the pressure-thickness relationship.

Sinus bradycardia as a predictor of right coronary artery occlusion in patients with inferior myocardial infarction

Differentiation of right coronary artery (RCA) from left circumflex artery (LCxA) occlusion may be difficult since both can present an electrocardiographic pattern of inferior myocardial infarction (IMI). We studied 133 patients with IMI, 92 patients with RCA occlusion and 41 patients with LCxA occlusion. Risk factors such as previous MI, arterial hypertension, diabetes, smoking, and dislipemia, were similar for RCA and LCxA occlusions. Patients with RCA occlusion had a higher incidence of isolated IMI than patients with LCxA occlusion, 50% vs. 17%, respectively ( P<0.001). Arterial hypotension was more prevalent ( P<0.05) among patients with RCA (18%) rather than those with LCxA occlusion (2%). RCA occlusion presented an association with sinus bradycardia, an association not observed with LCxA occlusion (15% vs. 0%, respectively; P<0.01). Total atrioventricular block was only present among patients with RCA (18%). Proximal occlusions of the RCA presented lower heart rates (sinus bradycardia) than medial and distal occlusions (13% vs. 1% and 1%, respectively; P<0.0001 and P<0.001). Therefore, regarding patients with IMI: (1) sinus bradycardia is more frequent when the infarct-related artery is the RCA; (2) proximal occlusions of the right coronary predispose low heart rates; and (3) occlusion of the LCxA rarely induces sinus bradycardia.

Comparison of 18-lead ECG and selected body surface potential mapping leads in determining maximally deviated ST lead and efficacy in detecting acute myocardial ischemia during coronary occlusion

Kornreich identified 6 body surface potential mapping (BSPM) leads outside the standard 12-lead electrocardiographic (ECG) sites for optimal recognition of ST segment elevation (+) and depression (−) during acute ischemia in anterior, inferior, and posterior myocardial zones (A+, A-, I+, I-, P+, P-). No comparison has been made between the 6 selected BSPM leads and 18-lead ECG (12 + V 3–5R + V 7–9) in detecting acute myocardial ischemia during coronary occlusion. Continuous 18-lead ECG and 6 selected BSPM leads were recorded in 68 patients (77 vessels) undergoing coronary angioplasty during balloon occlusion. Ischemia was defined as ST segment deviation (ΔST) ≥ 100 μV ≥ 1 lead from the preinflation baseline. The 18-lead ECG was a more frequent source of the maximal ΔST lead during left anterior descending artery, right coronary artery, and left circumflex artery occlusion (71 [92%]) than the 6 selected BSPM leads (5 [7%]). The 18-lead ECG was more efficacious than the 6 selected BSPM leads for detecting acute myocardial ischemia in the group as whole. The 18-lead ECG was also more efficacious for detecting right ventricular ischemia associated with proximal right coronary artery occlusion and for detecting ST segment elevation during left circumflex artery occlusion. Our findings indicate that the 18-lead ECG is the most frequent source of maximally deviated lead and is more efficacious in detecting myocardial ischemia during balloon occlusion than the 6 selected BSPM leads. The 6 selected BSPM leads do not add information above and beyond the 12- or 18-lead ECG, and thus cannot be recommended as optimal sites for continuous ST segment monitoring of patients with acute coronary syndromes.