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PubMed1984

Unipolar electrode system for an implantable defibrillator: new experimental approaches.

Defibrillation thresholds are studied in normal dog hearts after induction of ventricular fibrillation by alternating current. Shocks of progressively increasing energies are tried after a period of 10 seconds of sustained ventricular fibrillation. The endocardial electrode system may be either unipolar or bipolar, the distal electrode being situated at the right ventricular apex. The results suggest that for an optimal capacitor in the range of 9-20 uF, unipolar shocks are more effective than bipolar shocks (3-10 versus 10-30 Joules). In addition, several cardiac arrhythmias, including rapid ventricular tachycardia, accelerated idioventricular rhythm, and transient AV block are frequently observed. We conclude that (1) an implantable unipolar endocardial defibrillator seems feasible; and (2) the design should include the appropriate circuits to treat the arrhythmias observed after the shocks.

Animals↗
PubMed2006

Spontaneous coronary artery dissection during a dobutamine stress echocardiography.

We report a case of a spontaneous dissection of the right coronary artery during a dobutamine stress echocardiography (DSE) study in a middle-aged male. Our patient experienced a severe retrosternal pain of abrupt onset during the DSE study, whereas EKG was evident of significant ST segment elevation in II, III, avF, and V5-V6 leads, followed by an accelerated idioventricular rhythm. Immediate coronary angiogram revealed a minor dissection of the distal part of the right coronary artery.

Aortic Dissection↗
PubMed2000

Failure of thrombolysis by streptokinase: detection with a simple electrocardiographic method.

OBJECTIVE: To determine whether simple, readily applicable ECG criteria will allow early prediction of inadequate (< TIMI 3) flow in the infarct related vessel in patients receiving thrombolytic treatment for acute myocardial infarction; and to determine the success of streptokinase in achieving adequate antegrade flow in the infarct related vessel two hours after starting treatment. DESIGN: Cohort study. SETTING: Regional cardiothoracic unit. PATIENTS: 100 sequential patients with acute myocardial infarction. INTERVENTIONS: Coronary angiography two hours after the initiation of thrombolytic treatment, proceeding to rescue angioplasty for inadequate flow in the infarct related vessel where appropriate. MAIN OUTCOME MEASURES: Sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of six ECG criteria for the detection of inadequate antegrade flow in the infarct related vessel. RESULTS: The ECG test that performed best as a positive test for < TIMI 3 flow in the infarct related vessel was < 50% resolution of the ST segment elevation in the worst lead and no accelerated idioventricular rhythm. This had a sensitivity of 81%, specificity of 88%, positive predictive value of 87%, negative predictive value of 83%, and overall accuracy of 85%. CONCLUSIONS: Sensitive, specific, and simple ECG criteria are defined for diagnosing failure of thrombolytic treatment with streptokinase. These allow the early detection of patients at high risk of further adverse events from a persistently occluded vessel. They may be used without recourse to sophisticated equipment or complex analyses. Such patients can then be considered for alternative treatments or enrollment into appropriate research protocols.

Adult↗
PubMed2000

Angiographic assessment of prospectively determined non-invasive reperfusion indices in acute myocardial infarction.

OBJECTIVE: To investigate the value of non-invasive reperfusion indices in acute myocardial infarction, avoiding the possible need for acute coronary angiography and subsequent angioplasty. DESIGN: In a prospective angiographic study, seven potential ECG or clinical markers of reperfusion were analysed in 230 patients with acute myocardial infarction. In all patients two 12 lead ECGs were used: the ECG on admission and the ECG immediately before coronary angiography. Non-invasive markers of reperfusion determined just before coronary angiography were prospectively correlated to thrombolysis in myocardial infarction (TIMI) flow. Data analysis correlated these non-invasive indices with coronary flow (analysis A: TIMI 2-3 v TIMI 0-1 flow; analysis B: TIMI 3 v TIMI 0-2 flow). RESULTS: A sudden decrease in chest pain was the most common sign of reperfusion (36%), followed by reduction in ST segment elevation by >/= 50% (30%), and the development of a terminal negative T wave (20%) in the lead with the highest ST segment elevation. Reduction in ST segment elevation by > or = 50% and the appearance of an accelerated idioventricular rhythm (AIVR) had the highest positive predictive value for reperfusion. For analyses A and B, the positive predictive values were 85% and 66% for resolution of ST segment elevation, and 94% and 59% for AIVR, respectively. The presence of three or more non-invasive markers of reperfusion predicted TIMI 3 flow accurately in 80% of cases. CONCLUSIONS: The prospective use of non-invasive indices of reperfusion is simple, practical, and can be of value in assessing coronary patency in patients admitted with acute myocardial infarction. Using these indices, discrimination between TIMI 0-1 and TIMI 2-3 flow can be made with good accuracy. However, TIMI 3 flow cannot be determined reliably. The use of such non-invasive indices depends on the goal of reperfusion.

Coronary Angiography↗
PubMed2000

Antiarrhythmic efficacy of dipyridamole in treatment of reperfusion arrhythmias : evidence for cAMP-mediated triggered activity as a mechanism responsible for reperfusion arrhythmias.

BACKGROUND: Intracellular calcium overload is believed to play an important role in development of reperfusion arrhythmias. Dipyridamole, an inhibitor of cellular uptake of adenosine, may prevent or terminate reperfusion arrhythmias by reducing intracellular calcium overload. METHODS AND RESULTS: First, we tested for a preventive effect of dipyridamole. Sixty-one patients who underwent primary PTCA for treatment of acute anterior wall myocardial infarction were enrolled in this prospective study. Patients were divided into dipyridamole (DP) and nondipyridamole (non-DP) groups. The 2 groups had similar baseline characteristics. In the DP group, dipyridamole 0.5 mg/kg was infused intravenously for 3 minutes immediately before reperfusion during primary PTCA. Arrhythmias after reperfusion were analyzed from continuous ECG recordings. None of the patients in the DP group (n=23) had accelerated idioventricular rhythms (AIVR) or ventricular tachycardia (VT). In contrast, 7 (18.4%) had AIVR and 3 (7.9%) had VT in the non-DP group (n=38; P<0.01). Second, we tested for a termination effect of dipyridamole. Dipyridamole 0.5 mg/kg was infused intravenously while continuous ECG recordings were obtained in 9 patients who had either sustained AIVR (n=7) or sustained VT (n=2) after reperfusion of occluded coronary artery. Arrhythmias were terminated in all patients. CONCLUSIONS: These results indicate that administration of dipyridamole can prevent and terminate reperfusion arrhythmias such as AIVR and VT. cAMP-mediated triggered activity may, at least in part, be responsible for reperfusion-induced AIVR and VT.

Adenosine↗
PubMed1975

Use of atropine in patients with acute myocardial infarction and sinus bradycardia.

Fifty-six patients with acute myocardial infarction complicated by sinus bradycardia (SB) were treated with intravenous atropine and monitored in a coronary care unit. Atropine decreased or completely abolished premature ventricular contractions (PVCs) and/or bouts of accelerated idioventricular rhythm in 27 of 31 patients (87%) and brought systemic blood pressure up to normal in 15 of 17 patients (88%) with hypotension. In addition, atropine administration was associated with improved atrioventricular conduction in 11 of 13 patients (85%) with acute inferior myocardial infarction associated with 2 degrees or 3 degrees atrioventricular block. Seven patients developed ten significant adverse effects: ventricular tachycardia or fibrillation in three, sustainedsinus tachycardia in three, increased PVCs in three, and toxic psychosis in one. These major adverse effects correlated with either a higher initial dose of atropine (i.e., 1.0 mg aa compared with the usual 0.5 or 0.6 mg) or a total cumulative dose exceeding 2.5 mg over 21/2 hours. Atropine is the drug of choice for management of patients with SB and hypotension and is effective in the treatment of ventricular arrhythmias as well as conduction disturbances in patients with inferior myocardial infarction. Serious adverse effects, however, preclude use of atropine without careful medical supervision.

Acute Disease↗
PubMed1994

Significance of arrhythmias during the first 24 hours of acute myocardial infarction treated with alteplase and effect of early administration of a beta-blocker or a bradycardiac agent on their incidence.

BACKGROUND: Although early intravenous beta-blocker therapy during acute myocardial infarction (AMI) reduces the incidence of fatal arrhythmias in patients not treated with thrombolytic agents, its antiarrhythmic effect in thrombolysed patients remains controversial. We investigated prospectively the arrhythmia incidence in 244 patients with AMI receiving alteplase and a double-blind randomized adjunctive therapy with intravenous atenolol, alinidine, or placebo. Moreover, the characteristics and prognostic significance of early arrhythmias and their relation with infarct size and coronary patency were evaluated. METHODS AND RESULTS: All patients underwent 24-hour Holter monitoring on day 1 and were clinically followed in the hospital for 10 to 14 days. Coronary angiography was performed on day 10 to 14. Atenolol and alinidine significantly decreased the basic heart rate without causing more sinus arrest or higher-degree atrioventricular block. The prevalence of atrial fibrillation in alinidine patients was lower than in the atenolol patients (P = .007) but not lower than in placebo patients (P = .11). There was no effect of either agent on the incidence and frequency distribution of ventricular or supraventricular premature beats or on the incidence and characteristics of nonsustained ventricular tachycardia, accelerated idioventricular rhythm, sustained ventricular tachycardia (VT), or ventricular fibrillation (VF). On day 1, seven VF episodes were recorded in six patients (2.5%) and five VT episodes in five patients (2%). VF always started at < 2.5 hours after start of thrombolytic treatment and VT always at > 2.5 hours (average of 6 hours). Five of the seven VF and three of the five VT episodes started with an R-on-T. However, for all VT, the morphology of the first beat was the same as that of the following beats, suggesting that the sustained arrhythmia was not induced by an extrasystole. After day 1 and before hospital discharge, VF and VT developed in one and six patients, respectively. Three of the seven patients who developed VF during the first 2 weeks underwent coronary angiography; all three had an occluded infarct-related artery. In contrast, only one of nine patients with early or late VT had an occluded vessel. Patients with VT and VF on day 1 had a significantly larger enzymatic infarct size than those without the arrhythmia (P = .02), and a similar trend was noted for VT or VF after day 1 (P = .19). However, none of the patients with VT or VF on day 1 developed a life-threatening arrhythmia later during the hospital stay. Also, none of the seven patients with VT or VF after day 1 had experienced a major rhythm disturbance during the first 24 hours. CONCLUSIONS: (1) Our data do not support the hypothesis that beta-blockers or bradycardiac agents might reduce the incidence of major arrhythmias when used in conjunction with thrombolytic therapy. (2) The pathogeneses of VT and VF early during AMI are clearly distinct. (3) VT or VF during the first 2 weeks is a marker for a larger infarct. (4) We could not detect a relation between malignant arrhythmias on day 1 and recurrences within the following 2 weeks.

Anti-Arrhythmia Agents↗
PubMed2002

The independent association of renal dysfunction and arrhythmias in critically ill patients.

STUDY OBJECTIVES: The purpose of this study was to quantify the impact of baseline renal dysfunction on incidence and occurrence of cardiac arrhythmias in the coronary ICU. BACKGROUND: Renal dysfunction is an established predictor of all-cause mortality in the ICU setting. We set out to evaluate the independent contributory effect of renal dysfunction to arrhythmias and mortality in this population. DESIGN AND SETTING: We analyzed a prospective coronary care unit registry of 12,648 admissions by 9,557 patients over 8 years at a single, tertiary center. An admission serum creatinine level was available for 9,544 patients. Those patients not receiving long-term dialysis were classified into quartiles of corrected creatinine clearance with cutpoints of 46.2 mL/min/72 kg (group 1), 63.1 mL/min/72 kg, and 81.5 mL/min/72 kg. Dialysis patients (n = 527) were considered as a fifth comparison group (group 5). MEASUREMENTS AND RESULTS: Baseline characteristics including older age, African-American race, diabetes, hypertension, history of previous coronary disease, and heart failure were incrementally more common with increasing renal dysfunction strata. There were graded, independent increased risks for accelerated idioventricular rhythm (relative risk [RR], 2.43; 95% confidence interval [CI], 1.40 to 4.20; p = 0.002), sustained ventricular tachycardia (RR, 2.07; 95% CI, 1.02 to 4.22; p = 0.04), ventricular fibrillation (RR, 2.42; 95% CI, 1.13 to 5.15; p = 0.02), and complete heart block (RR, 3.64; 95% CI, 1.77 to 7.48; p = 0.0004, group 5 vs group 1). CONCLUSIONS: We conclude that baseline renal function is a powerful, independent predictor of cardiac arrhythmias in the coronary ICU population.

Arrhythmias, Cardiac↗
PubMed2004

Intracoronary verapamil rapidly terminates reperfusion tachyarrhythmias in acute myocardial infarction.

BACKGROUND: The restoration of coronary flow after transient ischemia immediately induces life-threatening ventricular tachyarrhythmias. Although most of these arrhythmias disappear spontaneously, some of them induce serious hemodynamic changes. This retrospective study investigates the efficacy of therapy with intracoronary verapamil to terminate reperfusion-induced ventricular tachyarrhythmias in patients with acute myocardial infarction (AMI). METHODS AND RESULTS: Between February 1992 and February 2003, 390 patients with a diagnosis of AMI were enrolled into the study. All patients received mechanical revascularization therapy within 6 h of onset of symptoms, and 109 patients experienced reperfusion-induced tachyarrhythmias. A subset of these patients was treated with intracoronary verapamil (0.25 to 1.0 mg) to terminate the reperfusion-induced tachyarrhythmia. They were evaluated for immediate termination of the tachyarrhythmias, hemodynamic changes, resumption rates, and major complications. Thirty-one patients (28%) were treated with intracoronary verapamil for the immediate termination of reperfusion-induced ventricular tachyarrhythmias. These tachyarrhythmias included 6 premature ventricular contractions, 19 accelerated idioventricular rhythms, 3 ventricular tachycardias, 2 ventricular fibrillations (VFs), and 1 torsades de pointes. Intracoronary verapamil was effective in rapidly terminating all reperfusion-induced arrhythmias except for VFs. The side effects of treatment included temporary hypotension (two patients) and bradycardia (one patient), although all patients recovered spontaneously. No major complications were induced by the intracoronary use of verapamil, and no resumptions of arrhythmias were documented. CONCLUSION: Intracoronary administration of verapamil can safely terminate reperfusion-induced ventricular tachyarrhythmias in a rapid manner. However, this effect was not seen for reperfusion-induced VF.

Adult↗
PubMed1991

Reperfusion arrhythmias after thrombolysis. Electrophysiologic tempest, or much ado about nothing.

Arrhythmias that may accompany myocardial reperfusion have generated significant clinical interest. First, there were concerns, based on animal studies, that high-grade ventricular tachyarrhythmias would pose a serious threat following thrombolytic therapy to treat an evolving myocardial infarction. Second, lower-grade arrhythmias, such as accelerated idioventricular rhythm, were cited as useful, noninvasive markers of successful reperfusion. Critical review of the current data, however, indicates that arrhythmias following thrombolytic therapy for acute myocardial infarction are usually neither dangerous clinical events nor consistent markers of reperfusion.

Animals↗
PubMed1999

[Attenuation of reperfusion phenomenon by reperfusion using leukocyte-depleted blood during direct percutaneous transluminal coronary angioplasty for acute myocardial infarction].

Leukocytes are important in the occurrence of reperfusion injury in coronary intervention for acute myocardial infarction (AMI). This study compared reperfusion injury caused by reperfusion using leukocyte-depleted blood (LD) and that by conventional angioplasty (control) through the reperfusion phenomenon including reperfusion arrhythmia and additional ST elevation during direct percutaneous transluminal coronary angioplasty (PTCA) in 41 patients with 21 left anterior descending artery (LAD) lesions and 20 right coronary artery (RCA) lesions. LD was prepared from 20 ml of venous blood, 20 ml of mixed blood and 60 ml of arterial blood from the patients (LD group; LAD-LD: n = 10, RCA-LD: n = 10) which was passed through a leukocyte removal filter. The blood was injected from the tip of the balloon catheter at 10 ml/min during inflation for 10 min before balloon deflation. The control group (LAD-control: n = 11, RCA-control: n = 10) underwent conventional angioplasty. The appearance of reperfusion arrhythmia [atrioventricular block (AVB) > II, accelerated idioventricular rhythm (AIVR), ventricular tachycardia (VT), ventricular fibrillation (Vf)] and measurements of STmax deviation before and after reperfusion, the differences of the STmax deviation (delta ST) and additional ST elevation (LAD: > or = 0.5 mV increase of sigma ST in lead V1-V6, RCA: > or = 0.3 mV increase of sigma ST in lead II, III and aVF) were studied. The appearance of reperfusion arrhythmias was as follows; LAD-LD: AVB 0, AIVR 1, VT 1, Vf 0, LAD-control: AVB 0, AIVR 4, VT 2, Vf 1, NS, and RCA-LD: AVB 0, AIVR 0, VT 0, Vf 0, RCA-control: AVB 2, AIVR 0, VT 1, Vf 0, NS. There was no reperfusion arrhythmia in the RCA-LD group. There was no significant difference in the appearance of reperfusion arrhythmias between the LAD-LD and LAD-control or RCA-LD and RCA-control groups. Before reperfusion the STmax deviation (mV) was LAD-LD 0.86 +/- 0.46 vs LAD-control 0.74 +/- 0.49 and RCA-LD 0.29 +/- 0.18 vs RCA-control 0.15 +/- 0.09 and after reperfusion LAD-LD 0.63 +/- 0.35 vs LAD-control 0.81 +/- 0.49 and RCA-LD 0.13 +/- 0.15 vs RCA-control 0.20 +/- 0.12, respectively. There were no significant differences between LAD-LD and LAD-control or RCA-LD and RCA-control groups. delta ST (mV) was LAD-LD 0.23 +/- 0.56 vs LAD-control 0.07 +/- 0.60, p = 0.09 and RCA-LD 0.16 +/- 0.12 vs RCA-control 0.06 +/- 0.14, p = 0.002, respectively. The number of patients with additional ST elevation soon after reperfusion was LAD-LD 3 vs LAD-control 10, p < 0.05 and RCA-LD 0 vs RCA-control 8, p < 0.001, respectively.

Angioplasty, Balloon, Coronary↗
PubMed1999

Electrophysiology of arrhythmias.

In this review, a brief overview of the different arrhythmogenic mechanisms is given, emphasizing that the mechanisms for initiation and maintenance of tachyarrhythmias are often not the same. Normal automaticity in Purkinje fibers, surrounded by partially depolarized tissue providing entrance block, is most likely responsible for ventricular premature beats and enhanced automaticity can lead to (rare) cathecholamine dependent ventricular tachycardias. Abnormal automaticity in partially depolarized cells may underlie ectopic atrial tachycardias and accelerated idioventricular rhythms in the subacute phase of myocardial infarction. Triggered activity based on early afterdepolarizations may trigger torsade de pointes in both the congenital and acquired long QT syndrome. The various mutations, affecting both potassium and sodium channels, will be discussed. Cellular calcium overload, which may occur in digitalis intoxication, hypertrophy and heart failure, is the cause for delayed afterdepolarizations and triggered activity. Reentry, anatomical and functional, ordered or reentry, is by far the most common cause of both atrial and ventricular tachycardias and fibrillation. Special attention will be given to the phenomenon of "electrical remodeling" in which prolonged episodes of rapid electrical activity leads to changes in ion channel function, which in their turn cause long lasting electrophysiological alterations.

Arrhythmias, Cardiac↗
PubMed1979

[Aneurysm of the membranous septum, left ventricular-right atrial communication and arrhythmias].

An aneurysm of the membranous part of the interventricular septum associated with a complex congenital malformation of the endocardial cushions was diagnosed in a 39 year old woman who presented with syncope. Diagnosis was made by echocardiography and confirmed by angiography. The operative findings were: a double aneurysm of the membranous septum, a left ventricular--right atrial fistula and two hemivalves attached to papillary muscles. The usfulness of echocardiography in the diagnosis of aneurysm of the membranous interventricular septum and in the follow up of ventricular septal defects from which they arise is emphasised. The pathogenesis of the arrhythmias observed (accelerated idioventricular rhythm, reciprocating tachycardias and syncope possibly related to transient heart block) is discussed.

Adult↗
PubMed2001

Management of cardiac arrhythmias in acute coronary syndromes.

A variety of atrial and ventricular arrhythmias are encountered in patients with acute coronary syndromes. These include both brady and tachyarrhythmias of supraventricular and ventricular origin. Sinus bradycardia and atrial fibrillation are the most common of supraventricular origin. Ventricular arrhythmias that merit consideration include premature ventricular complexes, accelerated idioventricular rhythm, ventricular tachycardia, and ventricular fibrillation. Intraventricular and atrioventricular conduction blocks associated with acute coronary syndromes include bundle branch blocks, fascicular blocks, and various degrees of atrioventricular block. A review of management of these arrhythmias is presented.

Angina, Unstable↗
PubMed2002

[Effect of the bioantioxidant histochrome on myocardial injury in reperfusion therapy on patients with myocardial infarction].

AIM: To evaluate effects of histochrome on severity of reperfusion damage in opening of the coronary artery in patients with acute myocardial infarction (MI). MATERIAL AND METHODS: 86 acute MI patients were randomized into three groups. 26 patients of group 1 A received 100 mg histochrome 10 min before and 1 hour after intravenous bolus administration of thrombolytic streptokinase; 20 patients of group 1 B received histochrome by the same scheme on the disease day 1 followed by 100 mg/day for 10 days; 40 control patients have undergone thrombolysis without prophylactic histochrome. RESULTS: In the control group ventricular extrasystoles (VES) arose in 100% patients, in groups 1A and 1B--in 27%. The same picture was observed in relation to episodes of accelerated idioventricular rhythm. Coronary reperfusion was accompanied by fast dynamics of ST segment and ORS complex in the control group. MI focus measured by the Selvester ECG method was less in histochrome groups. After myocardial reperfusion malonic dialdehyde in the serum rose 6 times in the control groups and was slightly elevated in groups 1A and 1B. CONCLUSION: Preventive administration of histochrome before thrombolytic therapy to reperfuse myocardium diminishes reperfusion damage: inhibits activity of lipid peroxidation and development of necrosis focus in acute period of MI.

Antioxidants↗
PubMed2003

[A patient with giant cell myocarditis and myositis associated with thymoma and myasthenia gravis].

We report a 62-year-old man with giant cell myocarditis and myositis associated with thymoma and myasthenia gravis (MG). He was diagnosed as having MG and invasive thymoma at the age of 45. After he had a myasthenic crisis at the age of 61, tacrolimus was indicated in order to improve his neurological symptoms, in addition to glucocorticoid. Three months later, he was readmitted to our hospital complaining of general fatigue and dyspnea. Serum level of creatine phosphokinase (9,835IU/L) and myocardium-derived troponin T (3.24 ng/mL) were elevated, and the ECG showed atrioventricular dissociation and accelerated idioventricular rhythm. In spite of glucocorticoid pulse therapies and high-dose immunoglobulin therapies, he died of cardiac failure within a few days. Autopsy was done, and histological examination of the myocardium and the skeletal muscle showed massive necrosis with infiltration of inflammatory cells including giant cells. These findings constituted giant cell myocarditis and myositis. Although it has been suggested that myocardial disorders can often occur in patients with thymoma and/or MG, the mechanism involved is still unknown. This report may provide new knowledge about the pathophysiology of giant cell myocarditis and myositis associated with thymoma and MG.

Giant Cells↗
PubMed1992

[Reperfusion arrhythmias in acute myocardial infarction].

Twenty-seven patients with acute myocardial infarction (AMI), in whom infarct-related coronary artery was occluded and thrombolytic therapy or PTCA were performed, were studied. Reperfusion confirmed by immediate coronary angiography was achieved in 24 patients. Reperfusion arrhythmias (RA) occurred in 19(79.2%) of the patients, including ventricular arrhythmias in 13 (54.2%). Ventricular fibrillation (VF) and sustained ventricular tachycardia (VT) developed in 2(8.4%), and accelerated idioventricular rhythm in 5(20.8%); the latter showed a reliable indicator of coronary artery recanalization. Transient sinus bradycardia or AV block occurred in 10 (66.7%) of the 15 patients with inferior-posterior MI, which was an indicator of recanalization of coronary artery and salvage of myocardium in inferior-posterior MI. The occurrence of RA was not correlated with the duration of ischemia; ventricular RA was not related to the location of AMI and the occurrence and severity of ischemic arrhythmias before reperfusion. The patients with RA were treated with ordinary antiarrhythmic therapy, VF and sustained VT in 2 patients were converted by electric defibrillation. No death related to RA occurred. RA couldn't be prevented by lidocaine.

Aged↗
PubMed1991

[Indirect criteria of coronary reperfusion and permeability in patients with acute myocardial infarction who have received thrombolytic therapy].

OBJECTIVE: To evaluate the value of some indirect reperfusion signs (IRS) as markers of coronary artery patency in patients (PTS) with acute myocardial infarction (AMI) submitted to intravenous (IV) thrombolytic therapy (TT). DESIGN: Retrospective study, with analysis of the sensibility (S), specificity (SP) and predictive value (PV) of three IRS: 1. Pain and ST resolution in the first three hours; 2. Peak CK in the first 13 hours; 3. accelerated idioventricular rhythm (AIVR) in the first three hours. SETTING: Coronary Care Unit (CCU) of the Santo António Hospital and Hemodynamic Laboratory of the S. João Hospital, Oporto. PATIENTS: Sixty seven PTS (mean age 53.4 +/- 10.6 years) with confirmed AMI, 62 male and five female, 34 with anterior and 33 with inferior infarction, TT started in the first three hours of the beginning of symptoms in 34 PTS and from three to six hours in 33 PTS, all submitted to coronary angiography in the hospital setting (7.6 +/- 5.9 days after AMI). INTERVENTIONS: IV administration of 1,500,000 U of streptokinase (SK) in 47 PTS and 30 U of APSAC in 20 PTS, preceded by 200 mg IV prednisolone and oral 100 mg acetilsalicylic acid, and followed by IV heparin therapy. Continuous electrocardiographic monitoring, and serial 12 leads ECG and enzymatic assays (at start and 1, 3, 7, 13 and 25 hours of TT). Analysis of the correlation of the three IRS (isolated and in association) with coronary artery patency (TIMI 2 or 3). MEASUREMENTS AND RESULTS: The total patency rate was 79.1%; there was no statistically significant difference with regard to AMI location, time of symptoms onset (0-3 vs 3-6 hours) or thrombolytic agent (SK vs APSAC). The first and second IRS had a high S and a low SP; together S = 79.2%, SP = 64.3% and PV = 89.4%. The third IRS with the first and/or the second one had a low S (about 25%) but SP and PV of 100%. The coronary patency rate of PTS without IRS was always greater than 50%. CONCLUSIONS: The analysed IRS although not very reliable are useful when considered in association. It is possible to assess PTA with high probability of reperfusion if AIVR is present. The absence of IRS does not exclude coronary artery patency. There is still missing more reliable no-invasive reperfusion markers.

Adult↗