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PubMed2003

Usefulness of frequent arrhythmias after epicardial recanalization in anterior wall acute myocardial infarction as a marker of cellular injury leading to poor recovery of left ventricular function.

Ventricular arrhythmias are associated with epicardial reperfusion but may also be a sign of cellular injury, which affects recovery of left ventricular (LV) function. To assess the correlation between reperfusion arrhythmias and the change in LV function after the acute phase in reperfused acute myocardial infarction (AMI), 62 patients with reperfused anterior wall AMI were studied. All patients underwent 24-hour Holter recording, echocardiography, and coronary angiography during the acute phase of AMI. Echocardiography was repeated at 1 to 2 months after AMI. Correlations between ventricular arrhythmias in the reperfusion phase and the change in LV wall motion score (WMS) during follow-up were studied. The number of reperfusion arrhythmias was significantly higher in patients with further deterioration of LV function; there were 5-, 14-, 131-, and 11-fold increases in isolated premature ventricular complexes (PVCs), PVCs in couplets, PVCs in bigeminy, and total PVCs, respectively, in patients with further increases in WMS after the acute phase. The incidence of repetitive, frequent, and early accelerated idioventricular rhythms (AIVRs) was correlated significantly with the change in LV function, with 129- and 105-fold increases in numbers of early AIVRs and total AIVRs, respectively, in patients with further worsening of LV function during follow-up. The incidence and the number of long-lasting nonsustained ventricular tachycardias as well as the number of rapid ventricular tachycardias and total ventricular tachycardia episodes were also correlated significantly with further deterioration. Thus, frequent arrhythmias associated with epicardial reperfusion strongly correlate with further worsening of LV function after the acute phase of AMI. This supports the hypothesis that these reperfusion arrhythmias are probably a noninvasive marker of cellular injury.

Adult↗
PubMed2000

A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty.

BACKGROUND: Different electrocardiographic changes have been described during thrombolytic therapy for acute myocardial infarction to indicate successful reperfusion. The occluded coronary artery also can be reopened by percutaneous transluminal coronary angioplasty (PTCA). This study was performed to compare electrocardiographic changes during primary or rescue PTCA and thrombolytic therapy. The electrocardiographic changes were studied directly at the moment of reperfusion during PTCA. METHODS AND RESULTS: Continuous 12-lead electrocardiographic monitoring was performed in 110 patients with acute myocardial infarction undergoing a reperfusion intervention (thrombolytic therapy or primary or rescue PTCA) to assess electrocardiographic changes during reperfusion. Patency and Thrombolysis In Myocardial Infarction flow in the infarct-related artery were assessed by coronary angiography. During reperfusion of the infarct-related coronary artery, early signs of reperfusion were an increase of ST-segment deviation (30%), ST-segment normalization (70%), and terminal T-wave inversion (60%); only 11% of patients showed no ST-segment changes. Thrombolytic therapy was significantly more often accompanied by a transient increase in ST-segment deviation compared with primary PTCA. Accelerated idioventricular rhythm was documented in 51%, an increase in the number of ventricular premature complexes in 42%, nonsustained ventricular tachycardia in 7%, and bradycardia in 18% of all patients. CONCLUSIONS: This study confirms the occurrence of specific electrocardiographic changes at the time of reperfusion. The pattern of ST-segment change upon reperfusion relates to the type of treatment. Awareness of electrocardiographic changes at the moment of reperfusion will help to select patients for rescue PTCA and can be used to assess the effect of future pharmacologic interventions to limit reperfusion damage.

Angioplasty, Balloon, Coronary↗
PubMed1995

Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction.

Continuous 12-lead electrocardiographic monitoring was performed in 61 patients receiving thrombolytic therapy for an acute myocardial infarction. Coronary angiography within 90 minutes revealed a patent vessel (Thrombolysis in Myocardial Infarction [TIMI] trial 2 or 3) in 44 patients. Early signs of reperfusion were ST-segment normalization (likelihood ratio 16.0), development of terminal T-wave inversion (likelihood ratio 10.6), accelerated idioventricular rhythm (likelihood ratio 6.0), and a twofold increase in ventricular premature complexes (likelihood ratio 2.5). Relief of chest pain after 60 minutes was reported by 96%. During reperfusion of the infarct-related vessel, an increase in ST-segment deviation was recorded in 61% of the patients, whereas 69% had an increase in chest pain preceding the eventual decline.

Arrhythmias, Cardiac↗
PubMed1984

Ventricular fibrillation and transient arrhythmias after defibrillation in patients with acute myocardial infarction.

Ventricular fibrillation (VF) and transient arrhythmias after defibrillation were analyzed from the recordings of 28 patients containing at least one episode of ventricular fibrillation. An R-on-T extrasystole initiated VF in 60% of the episodes. Other initiating factors were a late premature beat (24%), stable ventricular tachycardia (VT) (7%), accelerating idioventricular rhythm (5%) and cardioversion of VT (5%) with a sinusoidal waveform. After the initiating beat, in most cases, evidence was found of a transient ventricular tachycardia which then deteriorated into VF. With a stable VT this may occur after a long time; in the case of apolymorphic VT (with changing amplitude) it generally occurred within 30 s. The main transient arrhythmias generated by circulatory arrest during VF and by the defibrillation shock were: total arrest, total AV-block and/or bradycardia. The combination of a longer duration of VF and a high energy level generally resulted in an increase in the duration of these arrhythmias (P less than 0.01, N = 30). Comparison of episodes of VT and VF recorded in a single patient also shows that arrhythmias are more unfavourable and of longer duration after VF than after VT. These data emphasize fast defibrillation, initially with stored energy levels less than 250J.

Adult↗
PubMed1986

Effects of diltiazem on reperfusion-induced arrhythmias in vitro and in vivo.

The effects of the calcium antagonist, diltiazem, on myocardial injury during ischemia and reperfusion were studied both in vitro, in the isolated rat heart, and in vivo, in a closed-chest pig model. In the isolated rat heart, administration of diltiazem before or at the onset of ischemia resulted in a dose-dependent reduction of the incidence and duration of ventricular fibrillation. This reduction was associated with a dose-dependent reduction in overflow of ATP catabolites (adenosine, inosine, hypoxanthine and xanthine). Both changes were significant at concentrations of 3 X 10(-7) M diltiazem and higher. When 3 X 10(-7) M diltiazem was administered upon reperfusion no effect on the incidence of ventricular fibrillation and on ischemia induced total purine overflow was observed. However, the duration of ventricular fibrillation and purine overflow at 5 min after reperfusion were significantly reduced. In the pig experiments all untreated animals (n = 8) showed accelerated idioventricular rhythm (AIVR) upon reperfusion which lasted for 22 +/- 5 min after which sinus rhythm returned. Only two out of five treated animals (450 micrograms/kg/2 h) had an AIVR. Upon reperfusion both groups showed a substantial rise in noradrenaline concentration in the coronary sinus blood, but after 5 min this was significantly less in the treated group. Creatine kinase-kinetics were not altered by diltiazem, but the maximum creatine kinase level was significantly reduced. Within 4 days after the acute experiment 50% of the untreated animals died suddenly, whereas no sudden deaths occurred in the diltiazem group (P less than 0.05). Seven days after the acute experiment, sustained ventricular tachycardia could be induced with programmed electrical stimulation in three out of four surviving untreated pigs. In none of the diltiazem treated pigs was ventricular tachycardia inducible. The results of this study show that the calcium antagonist diltiazem can beneficially influence the events during ischemia and during reperfusion, both in vitro and in vivo; this benefit is associated with a reduction of ATP catabolism, creatine kinase release and noradrenaline overflow. Furthermore, diltiazem reduces electrical instability in the chronic phase of myocardial infarction.

Adenosine Triphosphate↗
PubMed1989

Associated reactions during and immediately after rtPA infusion.

The complications of IV recombinant tissue-type plasminogen activator (rtPA) have not been previously reported specifically for the first hours after initiation of the therapy when patients are often in emergency departments or in transport. The charts of 124 patients who received rtPA between April 1986 and December 1987 were retrospectively reviewed for reactions associated with rtPA infusion occurring in the first ten hours after the onset of rtPA administration. Minor bleeding developed in 19% of the patients, and life-threatening bleeding in 3%. Half of the life-threatening bleeding episodes were not predictable by history or physical examination. Arrhythmias were frequent despite the fact that all patients were maintained on IV lidocaine. New premature ventricular contractions occurred in 67%, accelerated idioventricular rhythm in 34%, ventricular tachycardia in 30%, and ventricular fibrillation in 2%. Many of the arrhythmias other than ventricular fibrillation had little hemodynamic consequence and did not require treatment. Neurologic episodes occurred in 3%, including two patients with intracerebral bleeding (1.5%); hypotension requiring treatment developed in 3%; and minor symptoms of allergy in 2%. Administration of rtPA in the ED requires careful patient selection to avoid bleeding complications and close monitoring to detect arrhythmias and changes in vital signs.

Arrhythmias, Cardiac↗
PubMed1987

Effect of metaraminol during acute inferior wall myocardial infarction accompanied by hypotension: preliminary study.

This study was designed to evaluate the effects of metaraminol (Aramine) in six patients with evolving acute inferior wall myocardial infarction accompanied by hypotension and warm limbs. There were 16 episodes of acute inferior wall ischemia, and the response to therapy was judged by evaluating blood pressure and ST segment and T wave abnormalities. Three patients received intravenous isosorbide dinitrate and two received streptokinase as the initial therapy. The mean ST segment elevation was significantly reduced (from 4.94 +/- 1 to 0.5 +/- 0.7 [p less than 0.0001]) after metaraminol infusion was initiated. The average T wave height also decreased (from 6.8 +/- 2 to -1.3 +/- 2.5 mm [p less than 0.0005]). The average heart rate decreased from 82 +/- 11 to 69 +/- 9 beats/min (p less than 0.05) and the mean arterial blood pressure increased from 81 +/- 12 mm Hg before metaraminol treatment to 126 +/- 8 mm Hg after treatment. All these changes occurred within a few minutes after metaraminol therapy was instituted. In 12 episodes, accelerated idioventricular rhythm appeared concomitantly with the resolution of ST segment elevation. Coronary angiography performed between 4 and 10 days after admission demonstrated significant obstruction in all infarct-related arteries, but none was totally occluded. Left ventricular function was normal in three patients and slightly hypokinetic in the inferior wall in two. These results indicate that in a selected group of patients with acute inferior myocardial infarction, metaraminol administration (in certain hemodynamic circumstances) can alleviate acute ischemia within a few minutes and thereby reduce ischemic injury.

Adult↗
PubMed2001

Usefulness of reperfusion ventricular arrhythmias in non-invasive prediction of early reperfusion and sustained coronary artery patency in acute myocardial infarction.

BACKGROUND: Established tenets of occurrence of reperfusion ventricular arrhythmias in acute myocardial infarction (AMI) do not provide insight into the timing of achieving reperfusion or whether coronary artery patency is sustained. We assessed the significance of ventricular arrhythmias in the non-invasive prediction of timely reperfusion and sustained restoration of coronary patency after thrombolysis in patients with AMI. METHODS: 24-hour Holter monitors were placed in 163 patients with an AMI before administration of thrombolytic therapy. Patients were classified into 3 groups of early (within 2 hours) or late reperfusion, or no-reperfusion, according with clinical and continuous ST-segment electrocardiographic criteria. Ventricular fibrillation, ventricular tachycardia (VT) and accelerated idioventricular rhythm (AIVR) were also categorized as having occurred early (within the first 2 hours) or late (after the first 2-hour period). Angiographic confirmation of coronary patency was determined 2 to 6 days after AMI. RESULTS: Early reperfusion was predicted by early sustained AIVR in 86% of patients and early non-sustained AIVR in 62.5% of patients, with sensitivity 38% and 77%, and specificity 96% and 69%, respectively; p<0.0001. Late non-sustained AIVR was commonly seen in early and late reperfused patients (92-97%) as well as in non-reperfused patients (74%). Sustained coronary patency was predicted by early sustained AIVR in 93% of patients, as well as by early non-sustained AIVR in 86% of patients and late non-sustained AIVR in 79% of patients, with sensitivity 22%, 55% and 94%, and specificity 95%, 71% and 18%, respectively; p<0.05. CONCLUSION: Only the occurrence of sustained AIVR, and probably early non-sustained AIVR convey useful information about both early reperfusion and sustained coronary artery patency. The absence of AIVR does not preclude successful thrombolysis.

Adult↗
PubMed2000

The use of the electrocardiogram to identify epicardial coronary and tissue reperfusion in acute myocardial infarction.

The standard 12-lead electrocardiogram (ECG) gives us crucial information concerning myocardial perfusion and the success of reperfusion therapy for ST elevation acute myocardial infarction. Continuous monitoring has advantages over repeated snapshot recordings. There are four electrocardiographic markers for prediction of the perfusion status of the ischemic myocardium: (1) ST-segment measurements, (2) T-wave configuration, (3) QRS changes, and (4) reperfusion arrhythmias. Complete and stable (> or = 70%) resolution of ST-segment elevation is associated with better outcome and preservation of left ventricular function than partial (30 to 70%) or no (<30%) ST-segment resolution. Early inversion of the T waves after initiation of reperfusion therapy is another marker of myocardial reperfusion and a good prognostic sign. Using standard 12-lead ECG, dynamic changes in Q-wave number, amplitude, and width; R-wave amplitude; and S-wave appearance are detected during reperfusion therapy. However, the significance of these changes has not been clarified. Reperfusion arrhythmias, especially bradycardia and accelerated idioventricular rhythm, are detected occasionally during reperfusion therapy, but the value of reperfusion arrhythmias as a marker of coronary artery patency is still debatable. Dynamic changes in the QRS complexes, ST segments and T waves occur during reperfusion therapy and the days after. Whereas changes in ST-segment amplitude have been extensively studied, the significance of QRS-complex and T-wave changes is less clear, and especially whether changes in the QRS complex and T wave may be complementary and additive to ST-segment monitoring. It has remained unclear whether electrocardiographic signs of reperfusion and reischemia should be used for therapeutic decision making in the clinical setting.

Electrocardiography↗
PubMed2000

The use of the electrocardiogram to identify epicardial coronary and tissue reperfusion in acute myocardial infarction.

The standard 12-lead ECG gives us crucial information concerning myocardial perfusion and the success of reperfusion therapy for ST-elevation acute myocardial infarction. Continuous monitoring has advantages over repeated snapshot recordings. There are four electrocardiographic markers for prediction of the perfusion status of the ischemic myocardium: 1) ST-segment measurements; 2) T-wave configuration; 3) QRS changes; and 4) reperfusion arrhythmias. Complete and stable (> or = 70%) resolution of ST-segment elevation is associated with better outcome and preservation of left ventricular function than partial (30% to 70%) or no (< 30%) ST-segment resolution. Early inversion of the T-waves after initiation of reperfusion therapy is another marker of myocardial reperfusion and a good prognostic sign. Using standard 12-lead ECG, dynamic changes in Q-wave number, amplitude and width, R-wave amplitude and S-wave appearance are detected during reperfusion therapy. However, the significance of these changes have not been clarified. Reperfusion arrhythmias, especially bradycardia and accelerated idioventricular rhythm are detected occasionally during reperfusion therapy, but the value of reperfusion arrhythmias as a marker of coronary artery patency is still debatable. Dynamic changes in the QRS complexes, ST-segments and T-waves occur during reperfusion therapy and the days after. While changes in ST-segment amplitude have been extensively studied, the significance of QRS-complex and T-wave changes are less clear, and especially whether changes in the QRS-complex and T-wave may be complementary and additive to ST-segment monitoring. It has remained unclear whether electrocardiographic signs of reperfusion and re-ischemia should be used for therapeutic decision-making in the clinical setting.

Animals↗
PubMed1993

Is arrhythmogenicity related to the speed of reperfusion during thrombolysis for myocardial infarction?

The objective of this study was to relate the number of ventricular arrhythmias (VA) to the normalization time of the ST segment during thrombolysis for acute myocardial infarction. The 24 h Holter recordings, begun on start of intravenous thrombolytic therapy, and the 12-lead electrocardiograms of 41 patients with a patent infarct-related artery according to coronary angiography were analysed. The mean time from onset of chest pain to angiography was 30.5 +/- 3.1 h, < or = 24 h in 59%. The normalization time of the ST segment, assessed by the time of decrease of ST segment elevation from start of Holter recording to normal or steady state was < or = 60 min in 13 patients (group 1), 60 to 180 min in 15 patients (group 2) and > 180 min in 13 patients (group 3). The incidence of VA was similar in all groups, except for ventricular tachycardias (VT) > 15 beats (group 1:69%, group 2:13%, group 3:15%, P = 0.002). The frequency of accelerated idioventricular rhythms (AIVR), early AIVR (< or = 6 h) and of VT was significantly higher in group 1 than in group 3 with a 8-, 30- and 6-fold increase, respectively (back transformed mean). We conclude that the number of VAs is related to the normalization time of the ST segment during reperfusion. This may suggest that faster reflow is more arrhythmogenic.

Cardiac Complexes, Premature↗
PubMed1997

Changing characteristics and in-hospital outcome in patients admitted with acute myocardial infarction. Observations from 1982 to 1994.

BACKGROUND: During the past decade, various new treatments have become available for patients with acute myocardial infarction. The effects of these treatment modalities have been studied extensively in selected patient groups. These studies indicate that early diagnosis, risk stratification and prompt initiation of treatment are of crucial importance for optimal benefit. However, it is not known whether prognosis changed in all patients admitted with an acute myocardial infarction. Also, the characteristics of the infarct population may have changed over time because of new medication regimens, invasive interventions and awareness of the importance of risk factors. METHODS: We studied all patients admitted with acute myocardial infarction in 1982, 1988 and 1994. Information on baseline characteristics, clinical variables and all interventions was collected. FINDINGS: In those 3 years 223, 227 and 235 patients were admitted because of an acute myocardial infarction. Patients admitted in 1994 were older, more often female and less often had a previous cardiac history. More patients admitted in that year had previous balloon angioplasty and coronary bypass grafting. Smoking habits decreased during the past decade. In-hospital mortality was 38 (17%) in 1982, 23 (10%) in 1988 and 22 (9%) in 1994 (P < 0.05). Variables related to high risk for in-hospital death in 1982 were higher age, low systolic blood pressure, atrial fibrillation, absence of accelerated idioventricular rhythm, sustained ventricular tachycardia and signs of left ventricular dysfunction; in 1988 the occurrence of non-sustained ventricular tachycardia, Killip class more than I, the absence of thrombolytic therapy, percutaneous transluminal coronary angioplasty or coronary artery bypass grafting were independently related to in-hospital death. In 1994, high risk variables for in-hospital death were dyspnoea on admission, sustained ventricular tachycardia, female gender, higher creatinine on admission, and a previous cardiac history. INTERPRETATION: In-hospital mortality for unselected patients admitted with an acute myocardial infarction decreased between 1982 and 1988 and remained the same between 1988 and 1994, in spite of further ageing of the population. In the study period there has been a change in baseline characteristics and high risk variables for in-hospital death after myocardial infarction.

Aged↗
PubMed1994

Acute intervention with captopril during thrombolysis in patients with first anterior myocardial infarction. Results from the Captopril and Thrombolysis Study (CATS).

The study was designed to examine the safety and efficacy of acute interventional use of captopril on left ventricular volumes, ventricular arrhythmias and neurohormones during thrombolysis in patients with a first anterior myocardial infarction, within 6 h of onset of symptoms. Left ventricular dysfunction and prognosis after myocardial infarction can be improved by angiotensin converting enzyme inhibition started after the ischaemic phase. Experimental evidence suggests that intervention during thrombolysis may lead to even further benefit. In a randomized, double-blind placebo-controlled trial, 298 patients with a first anterior myocardial infarction, eligible for thrombolytic therapy were treated with captopril 6.25 mg or placebo, started immediately upon streptokinase infusion and titrated to 25 mg t.i.d.. The efficacy of captopril by an intention-to-treat-analysis to reduce left ventricular volumes, ventricular arrhythmias, neurohumoral activation and enzymatic infarct size was measured. During dose titration, mean blood pressure and heart rate were similar in both groups. However, hypotension after the first dose was reported in 18 patients on placebo and 31 patients on captopril (P < 0.05). At discharge, 80% of patients were on study medication. Left ventricular volumes were significantly increased in both groups at 3 months, but they tended to be lower in the captopril group; however, the differences were not statistically significant. The incidence of accelerated idioventricular rhythm and non-sustained ventricular tachycardia in captopril patients was lower than in placebo patients (P < 0.05), parallelled by transiently lower norepinephrine levels (P < 0.05) upon thrombolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Captopril↗
PubMed1984

Antiarrhythmic efficacy of combined intravenous and oral mexiletine in acute myocardial infarction. A double blind placebo-controlled study.

The antiarrhythmic efficacy of mexiletine in acute myocardial infarction (AMI) was studied in 99 patients randomized to mexiletine or placebo treatment. The loading dose was 250 mg i.v. and 400 mg orally followed by 200 mg orally 2 h later, and thereafter 200 mg t.i.d. up to 42 h. Arrhythmias occurring during 48 h were analysed from continuous electrocardiographic recordings. AMI was verified in 35 of 50 mexiletine patients and in 38 of 49 placebo patients. No deaths or instances of ventricular fibrillation occurred in the AMI patients. The number of patients who had any event of accelerated idioventricular rhythm (AIVR; P less than 0.05) runs of ventricular premature beats (VPBs; P less than 0.01), ventricular tachycardia (P less than 0.01) and Ron T beats (P less than 0.05) was smaller in the mexiletine group than in the placebo group. The number of all VPBs (P less than 0.05), hours with occurrence of AIVR (P less than 0.05), runs (P less than 0.01) and Ron T beats (P less than 0.05) was smaller in the mexiletine than in the placebo group. Serum levels of mexiletine tended to be low throughout the study. The half-life of the elimination was 13.7 +/- 7.2 h (means +/- S.D.). Adverse effects were infrequent, and the treatment was well-tolerated. Combined iv. and oral mexiletine prophylaxis significantly suppressed repetitive ventricular tachyarrhythmias and Ron T beats. However, no clinical benefit from mexiletine treatment could be shown in a coronary care unit with a low frequency of primary ventricular fibrillation.

Adult↗
PubMed1987

Acute changes in blood pressure as a cause of cardiac arrhythmias.

The effect of an acute change in blood pressure (BP) on ventricular ectopic activity and the influence of antiarrhythmic agents on this effect were examined in 24 patients. In 11 patients with premature ventricular complexes (PVCs), the BP was temporarily reduced by a sodium nitroprusside drip. In all of them the incidence of PVCs was reduced (or annihilated) by the induced hypotension. In 13 patients without ventricular ectopic activity, a metaraminol drip was given until either a PVC appeared or the systolic BP reached 200 mmHg, or symptoms appeared. In 12 cases at least one PVC appeared and in 8 of them the total number of PVCs was 13 or more, usually in the form of bigeminy. The repetition of the test following quinidine administration (serum quinidine level 1.7 +/- 0.5 ng ml-1) in 6 cases did not change this pattern, with one exception. It prevented the appearance of idioventricular accelerated rhythm in one case in whom this rhythm had been induced by the hypertension provocative test before the quinidine administration. All cases, in whom the test failed to induce more than 3 PVCs, had no cardiac problem at all. Six of the 8 cases in whom the test induced 13 or more PVCs had organic cardiac disease or palpitation. Other arrhythmias observed on BP elevation, were supraventricular extra beats, nodal escape rhythms and atrioventricular block. In one case with cardiomyopathy, the BP elevation was associated with early signs of heart failure that subsided quickly. In conclusion, acute elevation on BP may be associated with the generation of PVCs and its reduction with their reduction or disappearance.

Adult↗
PubMed1987

Concentration-dependent protection by captopril against myocardial damage during ischemia and reperfusion in a closed chest pig model.

We previously reported concentration-dependent protection of captopril against ischemia-reperfusion injury in the isolated rat heart. In order to study these effects in vivo, we developed a closed-chest pig model. Reversible occlusion of the left coronary artery was achieved with a PTCA catheter during one hour. Captopril (C) i.v. was given in two different concentrations (0.6 mg/kg/10 min + 0.3 mg/kg/2 hr and 6 mg/kg/10 min + 3.0 mg/kg/2 hr) during the experiments to 11 and 10 pigs, respectively, versus 12 controls, who received only saline. Due to malignant ventricular arrhythmias, nine pigs died during ischemia. At the end of the reperfusion period of two hours, eight pigs were alive in each group. In the C-treated pigs, maximum creatine kinase after two hours of reperfusion was significantly lowered to 6,337 +/- 709 U/L in the high dose group versus 8,285 +/- 851 U/L in the low dose group and 9,635 +/- 1,115 U/L in the saline group. A reduction of local inosine overflow in the coronary sinus was seen. Maximum noradrenaline overflow after 5 min reperfusion diminished dose-dependently to 695 +/- 284 and 3,129 +/- 1,728 pg/ml in the C treated groups versus 4,693 +/- 2,277 pg/ml in the saline group. Mean arterial blood pressure and cardiac output decreased significantly during ischemia and reperfusion, but no significant differences occurred between the treated and untreated groups. Reperfusion arrhythmias, mainly accelerated idioventricular rhythm disturbances, were comparable among the three groups. We conclude that in vivo administration of C reduces myocardial damage upon reperfusion after one hour of ischemia in a dose-dependent way.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of isradipine on hemodynamic parameters and ventricular tachycardia in healed myocardial infarction.

The calcium-entry blocker isradipine was tested in a closed-chest pig model for chronic myocardial infarction. Ischemia was evoked in anesthetized pigs (25-35 kg) by inflating a catheter balloon in the left anterior descending coronary artery for at least 45 min. Hemodynamic monitoring and signal averaging of X, Y, and Z electrocardiographic leads were performed (150 beats, filtered at 50 Hz). After reperfusion, all animals developed an accelerated idioventricular rhythm and high creatine kinase (CPK) plasma levels. Coronary venous purines and catecholamines increased transiently. Two hours after reperfusion, heart rate was elevated from the initial 87.5 +/- 6.3 to 126 +/- 6.4 beats/min (p less than 0.01) and the pressure-rate product (PRP, an index of oxygen demand) from 9,530 +/- 630 to 11,950 +/- 790 mm Hg/min (p less than 0.05). After 2 weeks, six surviving pigs had a decreased stroke volume (98 +/- 18 versus the initial 124 +/- 14 microliters/kg, p less than 0.05), a prolonged high-frequency signal-averaged QRS duration (81.2 +/- 6.5 versus 65.7 +/- 2.9 ms, initially; p less than 0.05), and ventricular tachycardias (VTs), inducible by programmed electrical stimulation (PES). After the infusion of isradipine (1 microgram/kg/min for 30 min), the cardiac index increased from 92 +/- 14 to 133 +/- 8.7 ml/min.kg (p less than 0.02). Even at a higher heart rate, the PRP dropped from 12,600 +/- 1,900 to 10,560 +/- 1,400 mm Hg/min (p less than 0.05). Sustained monomorphic tachycardias were inducible in five pigs before and in three pigs after isradipine, and no deterioration of the signal-averaged electrocardiogram parameters was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Reperfusion arrhythmias during coronary angioplasty for acute myocardial infarction predict ST-segment resolution.

BACKGROUND: Despite early recanalization of an occluded infarct-related artery, myocardial reperfusion may remain impaired due to microvascular injury. Reperfusion arrhythmias may indicate successful microvascular reperfusion. METHODS: Microvascular reperfusion was assessed prospectively in 42 consecutive patients with ST-segment elevation acute myocardial infarction (AMI) by evaluation of the resolution of ST-segment elevation (<50% of initial level) immediately after successful coronary angioplasty. Patients were divided into two groups: those with ST resolution (n=24) and those without ST resolution (n=18). The presence of reperfusion arrhythmias immediately after recanalization was recorded. RESULTS: Patients with ST resolution were younger (54+/-12 years compared with 64+/-17 years, P=0.04), their pain-to-recanalization time was shorter (195+/-87 min compared with 294+/-179 min, P=0.05), they were less often diabetic (13% compared with 24%, P=0.05) and were more often given IIb/IIIa inhibitors (58% compared with 22%, P=0.02). Reperfusion arrhythmias were observed in 15 out of 24 patients with ST resolution (62%) but in only one out of 18 without ST resolution (5%) (P<0.01). Reperfusion arrhythmias included accelerated idioventricular rhythm, 13 (81%); multifocal ventricular premature beats, two (13%); and ventricular tachycardia, one (6%). The sensitivity and specificity of reperfusion arrhythmias for ST resolution were 62 and 95%, respectively. In a logistic regression model including age, time to treatment, diabetes, use of IIb/IIIa inhibitors and reperfusion arrhythmias, only the latter was found to be an independent predictor of ST resolution (P<0.01). CONCLUSION: Reperfusion arrhythmias following coronary angioplasty for AMI are a highly specific marker for ST resolution and may indicate successful microvascular reperfusion.

Adult↗