Synchronized coronary venous retroperfusion: protection from ischemia in coronary angioplasty (PTCA)]

The potentially ischemia-protective effect of ECG-synchronized coronary venous retroperfusion (SRP) with arterial blood via the coronary sinus (CS) was assessed in 26 patients (56 +/- 10 years, 22 male, 4 female) in the clinical scenario of PTCA of a proximal LAD stenosis. In six additional patients the SRP procedure failed due to anatomical or technical reasons. In an intraindividual comparison at least two standardized balloon inflations for 60 seconds at 6-8 atm were performed in randomized order with and without continuous SRP at a flow rate of 200 +/- 46 ml/min. Under both conditions echocardiographic regional wall motion, ST depression in leads V1-6, hemodynamic parameters and symptoms expressed in a pain score were continuously monitored during angioplasty. This study revealed that the echocardiographic regional wall motion score in the perfusion territory of the dilated artery increased from 1.65 +/- 1.81 at baseline to 5.65 +/- 2.88 (p < 0.001) during a one minute dilatation without SRP. With SRP-support the regional wall motion at 1 minute angioplasty was significantly improved to 3.55 +/- 2.80 (p < 0.025). Moreover, the ischemic ECG-changes were markedly less pronounced, whereas the subjective perception of anginal pain was not different as a function of SRP-support. Thus, the simultaneous coronary venous retroperfusion with arterial blood has ischemia-protective potential in elective PTCA of a proximal LAD stenosis and may reduce ischemic dysfunction with prolonged balloon inflations.     

Exogenous angiotensin II does not facilitate norepinephrine release in the heart

Studies on the effect of angiotensin II on norepinephrine release from sympathetic nerve terminals through stimulation of presynaptic angiotensin II type 1 receptors are equivocal. Furthermore, evidence that angiotensin II activates the cardiac sympathetic nervous system in vivo is scarce or indirect. In the intact porcine heart, we investigated whether angiotensin II increases norepinephrine concentrations in the myocardial interstitial fluid (NE(MIF)) under basal conditions and during sympathetic activation and whether it enhances exocytotic and nonexocytotic ischemia-induced norepinephrine release. In 27 anesthetized pigs, NE(MIF) was measured in the left ventricular myocardium using the microdialysis technique. Local infusion of angiotensin II into the left anterior descending coronary artery (LAD) at consecutive rates of 0.05, 0.5, and 5 ng/kg per minute did not affect NE(MIF), LAD flow, left ventricular dP/dt(max), and arterial pressure despite large increments in coronary arterial and venous angiotensin II concentrations. In the presence of neuronal reuptake inhibition and alpha-adrenergic receptor blockade, left stellate ganglion stimulation increased NE(MIF) from 2.7+/-0.3 to 7.3+/-1.2 before, and from 2.3+/-0.4 to 6.9+/-1.3 nmol/L during, infusion of 0.5 ng/kg per minute angiotensin II. Sixty minutes of 70% LAD flow reduction caused a progressive increase in NE(MIF) from 0.9+/-0.1 to 16+/-6 nmol/L, which was not enhanced by concomitant infusion of 0.5 ng/kg per minute angiotensin II. In conclusion, we did not observe any facilitation of cardiac norepinephrine release by angiotensin II under basal conditions and during either physiological (ganglion stimulation) or pathophysiological (acute ischemia) sympathetic activation. Hence, angiotensin II is not a local mediator of cardiac sympathetic activity in the in vivo porcine heart.     

Management of Patients with Heparin-Induced Thrombocytopenia: Focus on Recombinant Hirudin

It remains controversial whether percutaneous transluminal coronary angioplasty (PTCA) performed 24 hours after the onset of acute myocardial infarction (AMI) in coronary arteries with 99% stenosis is useful in preserving left ventricular function. We investigated the effectiveness of PTCA in preventing left ventricular remodeling when it was performed 24 hours after the onset of AMI in infarct-related coronary arteries (IRCAs) having 99% stenosis and thrombolysis in myocardial infarction (TIMI) grade 3 flow. The subjects were 19 patients with AMI (anterior wall, 9 patients; inferior wall, 7 patients; and non-Q, 3 patients) who, within 24 hours of the onset of AMI, underwent coronary angiography and left ventriculography during the acute and/ or chronic phases. The patients were divided into a PTCA group, comprised of patients in whom PTCA was successfully performed 24 hours after the onset of AMI (n = 10), and a non-PTCA group (n = 9). The non-PCTA group included patients who were successfully reperfused by thrombolysis and did not include patients who had spontaneous reperfusion or reperfusion after PTCA. In the non-PTCA group, the left ventricular end-diastolic volume (mean ± SD) was significantly increased in the chronic phase (86 ± 23 mL/m² as compared with the acute phase (67 ± 13 mL/m², whereas in the PTCA group no significant difference was observed between end-diastolic volumes in the acute and chronic phases (67 ± 26 and 68 ± 13 mL/m², respectively). Left ventricular remodeling is prevented by PTCA when it is performed 24 hours after the onset of AMI in IRCAs with 99% stenosis and TIMI grade 3 flow.     

Plasma catecholamines and N-terminal proBNP in patients with acute myocardial infarction undergoing primary angioplasty. Relation to left ventricular function and clinical outcome

BACKGROUND: Neither profiles nor prognostic values of neurohormonal markers have been prospectively evaluated in patients with acute myocardial infarction (AMI) undergoing primary angioplasty. METHODS AND RESULTS: In 118 consecutive patients with AMI undergoing successful reperfusion (TIMI 2 and 3) by primary angioplasty, plasma concentrations of norepinephrine, epinephrine and N-terminal proBNP (NT-proBNP) were measured before, 60 min and 10 days after angioplasty. Catecholamine concentrations (mean+/-SEM) rose to a maximum in the first hour after angioplasty (norepinephrine: 602+/-44 ng/L, epinephrine: 213+/-24 ng/L) and returned to normal at day 10. Conversely, NT-proBNP levels maintained a further increase from 799+/-44 pmol/L at baseline to 924+/-54 pmol/L at day 10. A NT-proBNP concentration above median at 60 min post-angioplasty predicted major adverse cardiac events (n=27) during the 18-36 month follow-up with an odds ratio of 5.9 (1.7-20.3) and was superior to catecholamines, to left ventricular ejection fraction and to other established postinfarction risk markers. CONCLUSIONS: In a low-risk cohort of patients with AMI undergoing successful reperfusion therapy, plasma NT-proBNP concentrations are elevated for at least ten days. The prognostic value of early plasma NT-proBNP should be further evaluated concerning its ability to facilitate risk stratification of infarct patients.     

AMI行直接与择期PTCA及冠状动脉内支架术中再灌注性心律失常的比较

目的对比直接与择期PTCA及冠状动脉内支架术中再灌注性心律失常的发生率及术后心肌功能的恢复。方法 63例行介入治疗的急性心肌梗死患者,随机分为AB两组。A组44例行择期PTCA加STENT术(经皮冠状动脉腔内成形加支架术);B组19例行直接PTCA加STENT术。术中分别应用CAG(冠状动脉造影术)定位IRA(梗塞相关动脉),多导心电生理仪观察再灌注性心律失常,根据不同的心律失常类型予以相应的处理。术后10～20d两组病人均做超声心动图,对比LVEF(左心室射血分数)以评价心肌功能恢复的情况。结果 (1)首次CAG显示A组IRA51支,其中左前降支(LAD)29支,右冠状动脉(RCA)15支,左回旋支(LCX)7支;B组IRA 24支,其中LAD 13支,RCA 7支,LCX 4支。两组冠状动脉分支梗塞率相比无显著差异(P>0.05)。(2)A B两组行PTCA加STENT术中再灌注性心律失常发生率,A组为25％(11/44),其中心室颤动发生率为14％(6/44);B组为79％(15/19),其中心室颤动发生率为53％(10/19)。两组再灌注性心律失常的发生率及心室颤动发生率相比均有显著性差异(P<0.05)。两组心室颤动病人行电除颤后均转复为窦性心率。(3)病人住院10～20d,二维超声心动图显示,LVEF达到或超过60％者。A组为64％(28例),B组为89％(17例)。两组相比有显著性意义(P<0.05)。结论 直接PTCA加STENT术     

Arterial and coronary sinus catecholamines in the course of spontaneous coronary artery spasm

We studied plasma catecholamine levels in 10 patients with frequent spontaneous episodes of coronary artery spasm to evaluate the role of the sympathetic nervous system. Peripheral venous norepinephrine in supine and upright postures, urinary excretion of catecholamines, and functional testing of the sympathetic nervous system did not differ from the same measurements in control subjects. Arterial and coronary sinus levels of norepinephrine and epinephrine drawn early in ischemia were not elevated over baseline; coronary sinus norepinephrine levels were higher than those in arterial samples and rose from 315 ± 32 (pg/ml ± SE) at the onset of ST elevation to 490 ± 49 pg/ml late in ischemia (p < 0.05). Plasma epinephrine levels, higher in arterial than coronary sinus samples, also rose significantly only late in ischemia, from 44 ± 14 pg/ml to 148 ± 35 pg/ml (p < 0.05) in arterial blood and from 33 ± 10 pg/ml to 108 ± 29 pg/ml in coronary sinus samples (p < 0.05). Generalized sympathetic nervous system activation is not likely to be the sole cause of coronary artery spasm.     

Effect of oral propranolol administration on azygos, renal and hepatic uptake and output of catecholamines in cirrhosis

Circulating catecholamines are increased in cirrhosis with portal hypertension, and increase further after propranolol. In 23 cirrhotic patients, plasma norepinephrine and epinephrine were determined in an artery, the azygos vein, the right renal vein and a hepatic vein before and after an oral 80-mg dose of propranolol. Baseline azygos and renal venous norepinephrine levels were significantly higher than arterial norepinephrine levels (+20%, p less than 0.005; and +28%, p less than 0.001, respectively). Hepatic venous norepinephrine and all venous epinephrine values were below the arterial values (all p less than 0.05). After propranolol intake, arterial norepinephrine and epinephrine increased (+16%, p less than 0.01; and +93%, p less than 0.001, respectively). Significant increases in norepinephrine and epinephrine were found in azygos and renal veins (all p less than 0.01), whereas hepatic venous norepinephrine and epinephrine remained unchanged. Azygos and hepatic blood flow decreased after propranolol intake (-27%, p less than 0.05; and -16%, p less than 0.01, respectively). Azygos spillover of norepinephrine (an estimate of locally released norepinephrine delivered to the circulation) and clearance of epinephrine remained unaltered. Hepatointestinal clearance showed no significant change for norepinephrine, but showed a borderline-significant decrease for epinephrine (-23%, p = 0.08). Our results show a net production of norepinephrine in the prehepatic splanchnic area drained through superior portalsystemic collaterals and in the kidneys. The increase in circulating catecholamines after propranolol intake is probably due to a combination of further enhancement of sympathetic activity and a decrease in catecholamine degradation.     

Coronary stenting for failed angioplasty in acute myocardial infarction

Intracoronary stents were implanted in 15 patients after unsuccessful PTCA in the setting of acute myocardial infarction (AMI). The stented vessel was the left anterior descending (LAD) in 11 patients, the right coronary artery (RCA) in 3 patients, and a venous bypass graft to the LAD in a single patient. A total of 16 stents were implanted (15 Palmaz-Schatz, Johnson and Johnson; and 1 Wiktor, Medtronic). Follow-up: 1 patient died 10 days after stent implantation as a result of renal failure and cardiogenic shock. Subacute thrombosis occurred in 2 patients, 5 and 15 days after stent implantation; both underwent successful emergency coronary artery bypass grafting (CABG). The remaining 12 patients were free from major ischemic events (death, AMI, and further revascularization) after a mean follow-up of 18.7 ± 4.1 months. We conclude that the long-term results of intracoronary stenting in AMI after failed PTCA are favourable. © 1996 Wiley-Liss, Inc.     

Continuous monitoring of coronary venous oxygen saturation during PTCA and its relation to electrocardiographic ST changes]

The purpose of this study was to investigate change in coronary venous oxygen saturation (CSO2-Sat) during percutaneous transluminal coronary angioplasty (PTCA) and to compare the results with those of standard 12-lead ECGs (s-ECG) and epicardial ECG induced using an intracoronary guidewire (ic-ECG). CSO2-Sat was measured continuously in 10 patients undergoing PTCA; 5 patients with lesions in the left anterior descending coronary artery (LAD), one with lesions in the left circumflex artery (LCX), and 4 with right coronary artery (RCA) lesions. The results were as follows: 1. In all 6 patients with stenotic lesions in the left coronary artery, CSO2-Sat decreased by 5 to 22% immediately after balloon inflation. Significant changes in ic-ECG (ST deviation > or = 0.1 mV) were observed in 5 of the 6 patients, while significant changes in s-ECG (ST deviation > or = 0.1 mV) were observed in only 3 of the 6 patients. The s-ECG did not seem to be sensitive enough to represent myocardial ischemia in the LCX. 2. The interval from the balloon inflation to the significant change was shorter for CSO2-Sat than for the ECGs in 4 of the 5 patients with LAD lesions, except Case 4. The recovery time of CSO2-Sat to the basal level on balloon deflation was longer than the recovery times of ic-ECG and s-ECG. 3. There was no significant change in the CSO2-Sat in 3 of the 4 patients undergoing PTCA for RCA lesions, while significant changes were observed in the ic-ECG and s-ECG in all 4 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

直接经皮腔内冠状动脉成形术对急性心肌梗塞QT离散度的影响

目的　研究急性心肌梗塞 (AMI)患者应用直接经皮腔内冠状动脉成形术 (PTCA)对 QT离散度(QTd)的影响。方法　回顾 95例 AMI患者 ,通过测量入院时及入院后不同时间心电图 ,计算校正 QTd(QTcd)。对比分析其中 68例 PTCA再通患者 (PTCA组 )与 2 7例未行 PTCA或溶栓患者 (对照组 )不同时间 QTd与 QTcd的变化。结果　 PTCA组再通即刻 QTd、QTcd较再通前明显延长 (P<0 .0 1 ) ,2小时后恢复到入院时水平 ,4小时后较入院时明显缩短 (P<0 .0 1 ) ,以后 2 4小时内相对稳定。对照组入院后 2 4小时内 QTd、 QTcd变化不大 (P>0 .0 5 )。结论　 AMI患者应用成功的 PTCA治疗可以缩短心室复极的 QTd,但再灌注即刻可加重心室复极的 QTd     

Early referral for intentional rescue PTCA after initiation of thrombolytic therapy in patients admitted to a community hospital because of a large acute myocardial infarction

BACKGROUND: If no in-house facilities for percutaneous transluminal coronary angioplasty (PTCA) are present, thrombolytic therapy is the treatment of choice for acute myocardial infarction (AMI). A few studies have shown benefit from rescue PTCA in patients directly admitted to centers with PTCA facilities. The obvious question arises whether patients with AMI initially admitted to a community hospital can benefit from early transfer for intentional rescue PTCA. METHODS AND RESULTS: One hundred sixty-five patients were transferred early for intentional rescue PTCA from a community hospital at a distance of 20 miles. On arrival at the angioplasty center, bedside markers were used to determine reperfusion. In case of obvious reperfusion, no invasive procedure was done; otherwise, coronary angiography and rescue PTCA, if necessary, was performed. During transfer, 1 (1%) patient died and 15 (9%) patients had arrhythmic or hemodynamic problems. Median time delay between onset of chest pain and arrival at the community hospital and the PTCA center was 61 minutes (range 0 to 413) and 150 minutes (range 28 to 472), respectively. In 66 (40%) patients, reperfusion was diagnosed by noninvasive reperfusion criteria on arrival at the PTCA center (group 1). Ninety-eight (59%) patients without evident noninvasive criteria of reperfusion underwent angiography 187 median minutes after the onset of chest pain. Forty-one (25%) patients had Thrombolysis In Myocardial Infarction grade 3 flow, and no further intervention was performed (group 2). In the remaining 57 (35%) patients, rescue PTCA was performed, which was successful in 96% (group 3). In-hospital mortality rate was lowest in group 1 compared with the other 2 groups (0% vs 7% vs 11%; P <.05). Reinfarction was highest in group 1 compared with the other groups (17% vs 5% vs 2%; P <.01). No significant differences were found in coronary artery bypass grafting, stroke, or bleeding complications. The 1-year follow-up data showed low revascularization rates; 2 (1%) patients died after discharge from the hospital. CONCLUSIONS: Early transfer of patients with large AMI for intentional rescue PTCA can be done with acceptable safety and is feasible within therapeutically acceptable time limits and results in additional early reperfusion in 33% of patients. A large, randomized, multicenter trial is needed to compare efficacy of intravenous thrombolytic treatment in a community hospital versus early referral for either rescue or primary PTCA.     

Local beta-adrenergic blockade does not reduce infarct size after coronary occlusion and reperfusion: A study of coronary venous retroinfusion of metoprolol

Summary Previous studies have demonstrated pronounced ischemic zone myocardial concentrations of metoprolol following coronary venous retroinfusion in pigs with coronary artery ligation. The effect of coronary venous retroinfusion of metoprolol on myocardial infarct size was studied in 16 pentobarbital-anesthetized open-chest pigs undergoing 60-minute occlusion of the left anterior descending coronary artery followed by 3 hours of reperfusion. Pigs in the experimental group (n=8) were given 0.4 mg/kg (1.0 mg/ml) of metoprolol via the anterior interventricular vein over a period of 5 minutes, beginning immediately after coronary occlusion followed by 0.2 mg/kg/hr intravenously. Control pigs (n=8) received the same volume of saline as the treated group. The risk area and the necrotic area were assessed by monastral blue dye and triphenyl tetrazolium chloride staining, respectively. Metoprolol did not influence hemodynamics. Plasma concentrations of metoprolol were within therapeutic levels. The administration of the beta-blocker resulted in a trend toward reduced norepinephrine concentrations, both in the aorta and coronary vein after coronary occlusion, but it did not prevent norepinephrine overflow following reperfusion. Infarct size expressed as a percentage of the risk area was 77±11% in the control group and 75±12% (mean ± SD; NS) in the treated group. Thus, metoprolol retroinfusion did not reduce infarct size and did not prevent catecholamine overflow after reperfusion. It is concluded that the beneficial effects of metoprolol in acute infarction are probably unrelated to local beta-adrenergic blockade, at least in the pig, an animal with a paucity of coronary collateral blood flow.     

Effects of intracoronary low-dose enalaprilat as an adjunct to primary percutaneous transluminal coronary angiography in acute myocardial infarction

Bradykinin accumulation is a potent cardioprotective mechanism underlying angiotensin-converting enzyme (ACE) inhibition in ischemia and/or reperfusion injury. There is, however, concern about treatment with ACE inhibitors in the very early phase of acute myocardial infarction (AMI) due to adverse systemic hemodynamic effects. We tested the hypothesis that cardiac bradykinin metabolism can be influenced by very low doses of intracoronary ACE inhibitors without harmful systemic effects in patients with AMI. Twenty-two patients with AMI in Killip classes II to III who underwent primary percutaneous transluminal coronary angiography (PTCA) were randomized to intracoronary enalaprilat (50 μg) or saline, given immediately after reopening of the infarct-related artery. Hemodynamics and electrocardiograms were monitored continuously and samples for determination of ACE activity, angiotensin II, bradykinin, kininogen, and cardiac marker proteins were collected from pulmonary arterial and central venous blood. Enalaprilat had no adverse effects on systemic hemodynamics, but rather stabilized arterial pressure and cardiac rhythm during reperfusion. Enalaprilat induced a 70% reduction of ACE activity and a significant increase of bradykinin in pulmonary arterial blood. Angiotensin II was not significantly affected by enalaprilat either in pulmonary arterial or in central venous blood. Myoglobin release was lower and the duration of reperfusion arrhythmias was significantly reduced in the enalaprilat group (p <0.05). Thus, in this pilot study, intracoronary enalaprilat infusion in the infarct-related artery is feasible in the setting of primary angioplasty and is safe and well tolerated. Effective cardiac ACE inhibition can be achieved by low-dose intracoronary enalaprilat, which primarily causes a potentiation of bradykinin.     

beta-Endorphin-induced stimulation of central sympathetic outflow: beta-endorphin increases plasma concentrations of epinephrine, norepinephrine, and dopamine in rats

Intracisternal administration of synthetic human beta-endorphin (0.058-7.25 nmol) in chronically cannulated, conscious, freely moving, adult male rats increased plasma concentrations of epinephrine, norepinephrine, and dopamine in a dose-related manner. Epinephrine secretion was the most sensitive to the stimulatory effect of intracerebral beta-endorphin; plasma epinephrine increased transiently in response to 0.058 nmol. Of the three catecholamines, plasma epinephrine showed the greatest and most rapid response to the largest dose (7.25 nmol) studied. Plasma norepinephrine increased significantly in response to 1.45 nmol, peaking later than plasma epinephrine. Plasma dopamine increased only in response to the highest dose examined. These beta-endorphin effects on plasma catecholamines were inhibited by intraarterial naloxone (1.1 mumol/kg), supporting mediation at opioid receptors. Pretreatment with the ganglionic blocking agent chlorisondamine inhibited the responses of all three catecholamines to intracisternal beta-endorphin. Bilateral adrenal denervation completely prevented the plasma epinephrine response to beta-endorphin and blunted the plasma norepinephrine and dopamine responses. Prior intracisternal administration of hemicholinium-3 blocked the plasma responses of all three catecholamines to intracisternal beta-endorphin, providing evidence for the involvement of central cholinergic neurons in the mechanism mediating beta-endorphin-induced increases in plasma catecholamines. The data are consistent with the hypothesis that endorphins act at a presently unknown brain site(s) to increase the central sympathetic outflow to adrenal medulla and peripheral sympathetic nerve endings, thus stimulating peripheral catecholamine release and increasing plasma concentrations of epinephrine, norepinephrine, and dopamine.     

Systemic neurohumoral activation and vasoconstriction during pacing-induced acute myocardial ischemia in patients with stable angina pectoris

To identify the effect of myocardial ischemia on systemic neurohormones and vascular resistance, 32 untreated, normotensive patients with coronary artery disease underwent incremental atrial pacing until angina. Arterial and coronary venous lactate and arterial values of catecholamines and angiotensin II were determined at control, at maximal pacing rates, and at 1, 2, 5 and 30 minutes after pacing. Based on pacing-induced ST-segment depression (greater than or equal to 0.1 mV) or myocardial lactate production, or both, patients were selected as ischemic (n = 25) or nonischemic (n = 7). Baseline clinical and hemodynamic data were comparable. During pacing, chest pain was similar (20 ischemic vs 7 nonischemic patients). Also, hemodynamic measurements were comparable, except for contractility, which did not improve, and left ventricular end-diastolic pressure, which significantly increased in ischemic patients. Moreover, during ischemia arterial pressures increased significantly (13%) and systemic resistance increased from 1,470 +/- 60 (control) to 1,632 +/- 76 dynes.s.cm-5 5 minutes after pacing (p less than 0.05) in ischemic but not in nonischemic patients. Pacing did not affect neurohormones in nonischemic patients. In contrast, norepinephrine in ischemic patients increased significantly from 1.7 +/- 0.2 (control) to 2.6 +/- 0.3 (maximal pacing) and to 3.0 +/- 0.4 nmol/liter (1 minute after pacing), whereas angiotensin II levels increased from 6.2 +/- 1.4 (control) to 9.3 +/- 2.1 pmol/liter (1 minute after pacing, p less than 0.05). Epinephrine only increased during maximal rates (0.9 +/- 0.1 vs 0.6 +/- 0.1 nmol/liter at control, p less than 0.05). Thus, myocardial ischemia activates circulating catecholamines and angiotensin II, accompanied by systemic vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arterial-venous differences of plasma catecholamines in man

To investigate the relationship between forearm venous levels of catecholamines and systemic levels, simultaneous arterial and forearm vein blood samples were obtained from 14 subjects undergoing elective dental procedures and assayed with a sensitive and specific radioenzymatic assay. Baseline venous levels of norepinephrine were greater than arterial levels (305 ± 30 pg/ml versus 221 ± 18; ± SEM, p < .005). Conversely, arterial epinephrine levels were higher than venous (132 ± 17 pg/ml versus 80 ± 10; p < .005). There was a significant relationship between arterial and venous levels of both norepinephrine (r = .77, p < .01) and epinephrine (r = .67, p < .01). The arterial-venous epinephrine difference increased from the baseline value of 44 ± 14 pg/ml to 108 ± 16 (p < .005) by 3 min after subcutaneous injection of epinephrine (18 μg), but the arterial-venous difference returned to 65 ± 24 by 5 min after injection (p = NS versus baseline). These findings indicate that under the conditions of this study, forearm tissues produced more norepinephrine than they removed, but removed more epinephrine than they produced. Baseline venous and arterial levels were related; when epinephrine production was augmented, there was a short time lag for the venous epinephrine increase.     

Late angiographic follow-up after successful coronary arterial thrombolysis and angioplasty during acute myocardial infarction

Emergency percutaneous transluminal coronary angioplasty (PTCA) is accepted as an important reperfusion intervention for acute myocardial infarction (AMI). Although its primary success rate is well documented, the frequency of restenosis after this procedure is unclear. The frequency of restenosis was determined in patients undergoing emergency PTCA at least 6 months after PTCA was performed during AMI. Of 66 consecutive patients undergoing emergency PTCA, 25 had a second, elective catheterization at an average of 22 months after AMI and 6 underwent repeat catheterization because of recurrent chest pain. Restenosis of the PTCA site was found in 10 of the 31 patients (32%) restudied. Also, 14 (45%) of these 31 patients showed progression of narrowing in the non-infarct-related coronary arteries. In summary, patients in whom AMI is treated by PTCA are at risk for restenosis and for progressive narrowing of the non-infarct artery.     

Elevated catecholamines during cardiac surgery: consequences of reperfusion of the postarrested heart

This study determines whether reperfusion of the heart with elevated blood levels of epinephrine (E) and norepinephrine (NE) during cardiac surgery produces deleterious effects. The study was conducted in 60 patients undergoing coronary artery bypass surgery. Arterial catecholamine values increased significantly (p less than 0.05), from prebypass control levels of 152 +/- 29 and 327 +/- 30 pg/ml of E and NE, respectively, to 415 +/- 78 and 554 +/- 49 pg/ml, at initiation of perfusion of the heart after the aortic cross-clamp was removed. Serial measurement of arterial (A) and coronary sinus (CS) E, NE, potassium, lactate, PO2 and CK-MB revealed that during 10 minutes of reperfusion the heart extracted E (positive A-CS difference, p less than 0.05), but that the NE A-CS difference was 0. The CS effluent contained significantly (p less than 0.05) higher concentrations of potassium, lactate and CK-MB during reperfusion than before aortic occlusion. There was no significant correlation of arterial E and NE, CS E and NE or A-CS differences in E and NE with myocardial release of lactate, potassium or CK-MB. There was a weak association (r = 0.4, p less than 0.01) between coronary sinus CK-MB and aortic occlusion time. Maximal arterial E and NE values did not correlate with 10-hour postoperative (maximal) CK-MB values. These results indicate that reperfusion of the postarrested ischemic heart with high levels of endogenously released catecholamines does not worsen ischemia or contribute significantly to myocardial damage.     

Postischemic cell death in reperfused porcine hearts is not attenuated by the spin trap agent PBN during early reperfusion

Summary Ischemic, reperfused porcine hearts were used to investigate whether the spin trap agent PBN (N-tert-butyl-alpha-phenylnitrone) attenuates postischemic cell death by scavenging of free radicals. The left anterior descending coronary artery (LAD) was ligated distally in 16 pigs for 45 min and then reperfused for 3 h. PBN (coronary concentration approximately 1 mM) was infused into the LAD of eight pigs during the first 45 min of reperfusion. Electron spin resonance spectroscopy (ESR) was performed to identify free radical adducts in the reperfused coronary venous blood. Regional systolic shortening (SS%) was determined by sonomicrometry. Infarct size was evaluated as the percentage of infarcted (tetrazolium stain) to ischemic (dye technique) myocardium. The transmural ultrastructural degree of myocardial injury as well as myocardial ATP levels were assessed at the end of the experiment.Intracoronary treatment with PBN during early reperfusion did not attenuate myocardial damage. Infarct sizes (control group 59±19%, treated group 55±14%), transmural ultrastructural alterations, myocardial ATP concentrations (control group 1.8±0.3 mol/mg frozen weight, treated group 1.7±0.4 mol/mg) and regional systolic shortening at the end of the experiments (control group –1±5%, treated group –2±6% did not differ significantly. Furthermore, under various experimental conditions of spin trapping, free radical adducts could not be identified in coronary venous blood during early reperfusion. The results suggest that the spin trap agent PBN (1 mM) does not affect postischemic cell death in porcine hearts.This study was supported by the Deutsche Forschungsgemeinschaft (KL 724/1-2) and the SFB 330-Organprotektion, Göttingen (A8)     

Decreased interstitial glucose and transmural gradient in lactate during ischemia

Summary The purpose of this investigation was to assess the effects of ischemia and reperfusion on the transmural levels of glucose and lactate in the interstitium in 11 open-chest swine. Microdialysis probes were used to estimate changes in interstitial metabolities across the ventricular wall. Probes were placed in the subepicardium and the subendocardium of the left anterior descending (LAD) coronary artery perfusion bed and in the midmyocardium of the circumflex (CFX) perfusion bed. The LAD coronary artery was cannulated and perfused with blood from the femoral artery through an extracorporal perfusion circuit. Ischemia was induced in the LAD perfusion bed by reducing the flow of the LAD perfusion pump by 60% for 50 min, and was followed by 30 min of reperfusion. Regional myocardial blood flow was assessed with fluorescent microspheres. Ischemia resulted in a transmural gradient in blood flow, with the most severe reduction in flow occurring in the subendocardium (p<0.05). We found a significant reduction in interstitial glucose in both the LAD subepicardium (1.26±0.24 mM) (p=0.0009) and subendocardium (0.89±0.21 mM) (p=0.0001) during ischemia compared to the aerobic (non-ischemic) period (1.97±0.25 mM, 2.03±0.29 mM for the subepicardium and subendocardium, respectively). This coincided with a significant reduction in glucose delivery (LAD pump flow^* arterial glucose) to the LAD perfusion bed during ischemia (54.5±8.5 mol/min) compared to aerobic values (182.1±25.3 mol/min) (p<0.05). Interstitial lactate levels were significantly increased during ischemia in the LAD subendocardium (3.39±0.46 mM) compared to the aerobic values (1.73±0.46 mM) (p<0.0029). A transmural gradient in interstitial lactate levels was observed during ischemia: this gradient was not seen during the aerobic period and was negated upon reperfusion. In conclusion, ischemia resulted in a decrease in interstitial glucose in both the LAD subepicardium and subendocardium, and an increase in interstitial lactate in the LAD subendocardium. Further, a transmural gradient in interstitial lactate levels was observed during ischemia, with the highest lactate values appearing in the subendocardium.