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Background Ticagrelor was shown to reduce mortality in patients who underwent coronary artery bypass grafting (CABG), but its effect on graft patency is unknown. Methods We performed a prospective, randomised, double-blind, placebo-controlled trial, comparing ticagrelor 90 mg twice daily versus placebo for 3 months added to aspirin 81 mg/day, following isolated CABG. Aspirin was started within 12 h, and study medication within 72 h after CABG. Primary outcome was graft occlusion on CT angiography (CTA) performed 3 months post CABG. Patients were followed to 12 months for death, myocardial infarction, stroke, repeat revascularisation and bleeding. Results The study was terminated prematurely after randomising 70 patients between September 2011 and August 2014 because of slow recruitment. CTA was performed in 56 patients who completed >1 month of study drug. Graft occlusion occurred in 7/25 (28.0%) patients on ticagrelor and 17/31 (48.3%) on placebo, p=0.044. Of 207 analysable grafts, graft occlusion occurred in 9/87 (10.3%) with ticagrelor and 22/120 (18.3%) with placebo, p=0.112. Graft occlusion or stenosis ≥50% occurred in 10/87 (11.5%) ticagrelor vs 32/120 (26.7%) placebo, p=0.007. There was no major bleeding, but minor bleeding was higher with ticagrelor (31.4% vs 2.9%, p=0.003). In univariate analysis, ticagrelor use reduced graft occlusion (OR 0.32, 95% CI 0.10 to 0.97, p=0.047), which remained significant on multivariable analysis (OR 0.25, 95% CI 0.073 to 0.873, p=0.03). Conclusions Ticagrelor added to aspirin after CABG reduced the proportion of patients with graft occlusion, and was a significant univariate and multivariable predictor of graft occlusion. These results are hypothesis-generating and should be confirmed in larger studies. Trial registration number NCT01373411: Results.

Importance The majority of sudden and/or arrhythmic deaths (SAD) in patients with coronary heart disease occur in those without severe systolic dysfunction, for whom strategies for sudden death prevention are lacking. Objective To provide contemporary estimates of SAD vs other competing causes of death in patients with coronary heart disease without severe systolic dysfunction to search for high-risk subgroups that might be targeted in future trials of SAD prevention. Design, Setting, and Participants This prospective observational cohort study included 135 clinical sites in the United States and Canada. A total of 5761 participants with coronary heart disease who did not qualify for primary prevention implantable cardioverter defibrillator therapy based on left ventricular ejection fraction (LVEF) of more than 35% or New York Heart Association (NYHA) heart failure class (LVEF >30%, NYHA I). Exposures Clinical risk factors measured at baseline including age, LVEF, and NYHA heart failure class. Main Outcomes and Measures Primary outcome of SAD, which is a composite of SAD and resuscitated ventricular fibrillation arrest. Results The mean (SD) age of the cohort was 64 (11) years. During a median of 3.9 years, the cumulative incidence of SAD and non-SAD was 2.1% and 7.7%, respectively. Sudden and/or arrhythmic death was the most common mode of cardiovascular death accounting for 114 of 202 cardiac deaths (56%), although noncardiac death was the primary mode of death in this population. The 4-year cumulative incidence of SAD was lowest in those with an LVEF of more than 60% (1.0%) and highest among those with LVEF of 30% to 40% (4.9%) and class III/IV heart failure (5.1%); however, the cumulative incidence of non-SAD was similarly elevated in these latter high-risk subgroups. Patients with a moderately reduced LVEF (40%-49%) were more likely to die of SAD, whereas those with class II heart failure and advancing age were more likely to die of non-SAD. The proportion of deaths due to SAD varied widely, from 14% (18 of 131 deaths) in patients with NYHA II to 49% (37 of 76 deaths) in those younger than 60 years. Conclusions and Relevance In a contemporary population of patients with coronary heart disease without severe systolic dysfunction, SAD accounts for a significant proportion of overall mortality. Moderately reduced LVEF, age, and NYHA class distinguished SAD and non-SAD, whereas other markers were equally associated with both modes of death. Absolute and proportional risk of SAD varied significantly across clinical subgroups, and both will need to be maximized in future risk stratification efforts.

Background Hypertension is a well-established risk factor for myocardial infarction (MI), but its prognostic importance in survivors of an acute MI is less clear. Methods We used Cox proportional hazards models to examine the risk of any major cardiovascular event (cardiovascular death, heart failure, recurrent MI, or stroke)—combined or individual components—and all-cause death and evaluate the efficacy of captopril in 906 patients with hypertension and 1325 patients without hypertension in the Survival and Ventricular Enlargement (SAVE) clinical trial. All patients had survived an acute MI with resultant left ventricular (LV) systolic dysfunction, but without overt heart failure, and were randomized within 3 to 16 days after the index MI to receive either captopril or placebo. The mean (± SD) follow-up period was 42 ± 10 months. Results After adjustment for known risk factors, medication use at enrollment, and baseline systolic blood pressure, patients with hypertension had a significant increase in the risk of experiencing a combined cardiovascular event (47.7% vs 31.3%; hazard ratio [HR], 1.49; 95% CI, 1.28–1.74), cardiovascular death (23.4% vs 15.9%; HR, 1.40; 95% CI, 1.12–1.74), heart failure (27.7% vs 15.5%; HR, 1.64; 95% CI, 1.34–2.02), and all-cause death (27.4 vs 19.3%; HR, 1.25; 95% CI, 1.02–1.53), and a similar but statistically non-significant increase in the risk of non-fatal or fatal recurrent MI (17.4% vs 10.9%; HR, 1.27; 95% CI, 0.98–1.65), and non-fatal or fatal stroke (5.0% vs 3.6%; HR, 1.31; 95% CI, 0.81–2.09). Captopril resulted in similar benefits for both patients with and patients without hypertension. The number of combined cardiovascular events prevented for every 100 patients treated with captopril was 7.0 (95% CI, 0.5–13.5) in patients with hypertension and 7.5 (95% CI, 2.6–12.5) in patients without hypertension. Conclusions In survivors of an acute MI with LV systolic dysfunction, antecedent hypertension was associated with a greater risk of subsequent adverse cardiovascular events, not directly explained by elevated blood pressure levels. Captopril use was beneficial in both patients with and patients without hypertenson.

Background —The role of lipid modification in stroke prevention is controversial, although increasing evidence suggests that HMG-CoA reductase inhibition may reduce cerebrovascular events in patients with prevalent coronary artery disease. Methods and Results —To test the hypothesis that cholesterol reduction with pravastatin may reduce stroke incidence after myocardial infarction, we followed 4159 subjects with average total and LDL serum cholesterol levels (mean, 209 and 139 mg/dL, respectively) who had sustained an infarction an average of 10 months before study entry and who were randomized to pravastatin 40 mg/d or placebo in the Cholesterol and Recurrent Events (CARE) trial. Using prospectively defined criteria, we assessed the incidence of stroke, a prespecified secondary end point, and transient ischemic attack (TIA) over a median 5-year follow-up period. Patients were well matched for stroke risk factors and the use of antiplatelet agents (85% of subjects in each group). Compared with placebo, pravastatin lowered total serum cholesterol by 20%, LDL cholesterol by 32%, and triglycerides by 14% and raised HDL cholesterol by 5% over the course of the trial. A total of 128 strokes (52 on pravastatin, 76 on placebo) and 216 strokes or TIAs (92 on pravastatin, 124 on placebo) were observed, representing a 32% reduction (95% CI, 4% to 52%, P =0.03) in all-cause stroke and 27% reduction in stroke or TIA (95% CI, 4% to 44%, P =0.02). All categories of strokes were reduced, and treatment effect was similar when adjusted for age, sex, history of hypertension, cigarette smoking, diabetes, left ventricular ejection fraction, and baseline total, HDL, and LDL cholesterol and triglyceride levels. There was no increase in hemorrhagic stroke in patients on pravastatin compared with placebo (2 versus 6, respectively). Conclusions —Pravastatin significantly reduced stroke and stroke or TIA incidence after myocardial infarction in patients with average serum cholesterol levels despite the high concurrent use of antiplatelet therapy.

To the Editor: Proteinuria is a known predictor of cardiovascular (CV) morbidity and mortality in diabetics, hypertensive patients, and the general population ([1–3][1]), but the impact of proteinuria as a risk factor after acute myocardial infarction (MI) is less well-defined. We analyzed a

Background There is increasing evidence of a link between conduit vessel stiffness and cardiovascular events, although the association has never been tested in a large post–myocardial infarction patient population. Methods and Results We evaluated the relationship between baseline pulse pressure, measured by sphygmomanometry 3 to 16 days after myocardial infarction, and subsequent adverse clinical events in the 2231 patients enrolled in the SAVE Trial. Increased pulse pressure was associated with increased age, left ventricular ejection fraction, female sex, history of prior infarction, diabetes, and hypertension and use of digoxin and calcium channel blockers. Over a 42-month period, there were 503 deaths, 422 cardiovascular deaths, and 303 myocardial infarctions. Pulse pressure was significantly related to each of these end points as a univariate predictor. In a multivariate analysis, pulse pressure remained a significant predictor of total mortality (relative risk, 1.08 per 10 mm Hg increment in pulse pressure; 95% CI, 1.00 to 1.17; P P Conclusions These data provide strong evidence for a link between pulse pressure, which is related to conduit vessel stiffness, and subsequent cardiovascular events after myocardial infarction in patients with left ventricular dysfunction.

Objectives. This study attempted to evaluate whether neurohumoral activation at the time of hospital discharge in postinfarction patients helps to predict long-term prognosis and whether long-term therapy with the angiotensin-converting enzyme inhibitor captopril modifies this relation. Background. Neurohumoral activation persists at the time of hospital discharge in a large number of postinfarction patients. The Survival and Ventricular Enlargement (SAVE) study demonstrated that the angiotensin-converting enzyme inhibitor captopril improves survival and decreases the development of severe heart failure in patients with left ventricular dysfunction (left ventricular ejection fraction ≤40%) but no overt postinfarction heart failure. Methods. In 534 patients in the SAVE study, plasma neurohormone levels were measured a mean of 12 days after infarction. Patients were then randomized to receive captopril or placebo and were followed up for a mean (±SD) of 38 ± 6 months (range 24 to 55). The association between activation of plasma neurohormones at baseline and subsequent cardiovascular mortality or the development of heart failure was assessed with and without adjustment for other important prognostic factors. Results. By univariate analysis, activation of plasma renin activity and aldosterone, norepinephrine, atrial natriuretic peptide and arginine vasopressin levels were related to subsequent cardiovascular events, whereas epinephrine and dopamine levels were not. By multivariate analysis, only plasma renin activity (relative risk 1.6, 95% confidence interval [CI] 1.0 to 2.5) and atrial natriuretic peptide (relative risk 2.2, 95% CI 1.3 to 3.8) were independently predictive of cardiovascular mortality, whereas the other neurohormones were not. Only plasma renin activity and aldosterone, atrial natriuretic peptide and arginine vasopressin were independent predictors of the combined end points of cardiovascular mortality, development of severe heart failure or recurrent myocardial infarction. Except for 1-year cardiovascular mortality, the use of captopril did not significantly modify these relations. Conclusions. Neurohumoral activation at the time of hospital discharge in postinfarction patients is an independent sign of poor prognosis. This is particularly true for plasma renin activity and atrial natriuretic peptide. Except for 1-year cardiovascular mortality, captopril does not significantly modify these relations.

Background There are major differences in the organization of the health care systems in Canada and the United States. We hypothesized that these differences may be accompanied by differences in patient care. Methods To test our hypothesis, we compared the treatment patterns for patients with acute myocardial infarction in 19 Canadian and 93 United States hospitals participating in the Survival and Ventricular Enlargement (SAVE) study, which tested the effectiveness of captopril in this population of patients after a myocardial infarction. Results In Canada, 51 percent of the patients admitted to a participating coronary care unit had acute myocardial infarctions, as compared with only 35 percent in the United States (P

Background— Atrial arrhythmias (AA) are an important cause of morbidity after cardiac surgery. Efforts at prevention of postoperative AA have been suboptimal. Perioperative beta-blocker administration is the standard of care at many centers. Although prophylactic administration of magnesium sulfate (MgSO 4 ) has been recommended, review of all previously published trials of MgSO 4 reveals conflicting results. This study was designed to address methodological shortcomings from previous studies and is the largest randomized, placebo-controlled trial of intravenous (IV) MgSO 4 for the prevention of AA after coronary artery bypass grafting or cardiac valvular surgery. Methods and Results— A total of 927 nonemergent cardiac surgery patients were stratified into 2 groups: isolated coronary artery bypass grafting (n=694), or valve surgery with or without coronary artery bypass grafting (n=233), and randomized to receive either 5g IV MgSO 4 or placebo on removal of the cross-clamp, followed by daily 4-hour infusions, from postoperative day 1 until postoperative day 4. All patients were treated according to an established oral β-blocker protocol. Postoperative serum Mg levels were checked and standard of care was to administer IV MgSO 4 for low serum levels. The primary end point was AA lasting ≥30 minutes or requiring treatment for hemodynamic compromise. There were no differences in the incidence of AA between patients who received IV MgSO 4 or placebo (26.4% versus 24.3%, respectively). The results were similar when broken down according to stratified groups. Conclusions— In patients treated with a protocol for postoperative oral β-blocker after nonemergent cardiac surgery, the addition of prophylactic IV MgSO 4 did not reduce the incidence of AA.

Patients with New York Heart Association functional class II or III heart failure stabilized on furosemide therapy were entered into a randomized controlled trial comparing enalapril (n = 72) and digoxin (n = 73). End points were clinical outcome, treadmill exercise capacity and echocardiographic left ventricular dimensions. Improvement in clinical outcome was defined as a reduction of at least one functional class, and deterioration as an increase of at least one functional class or withdrawal because of an adverse clinical event.After 4 weeks, 13 patients receiving enalapril showed improvement, 55 had no change and 9 manifested deterioration compared with 7, 49 and 17, respectively, in the digoxin group (p < 0.01). After 14 weeks, 13 patients receiving enalapril showed improvement, 50 had no change and 9 manifested deterioration, compared with 14, 37 and 22, respectively, in the digoxin group (p < 0.025). More patients in the digoxin group were withdrawn because of an adverse clinical event (p < 0.05).Exercise time and percent fractional shortening improved in both groups (p < 0.001 and 0.50). Both rate-pressure product and subjectively evaluated exertion during submaximal exercise were reduced only in the enalapril group. Although the majority of patients in both groups did well, those receiving enalapril experienced fewer adverse clinical events and had less fatigue during submaximal exercise.

Background. Despite the fact that coronary artery disease is the leading cause of death among women, previous studies have suggested that physicians are less likely to pursue an aggressive approach to coronary artery disease in women than in men. To define this issue further, we compared the care previously received by men and women who were enrolled in a large postinfarction intervention trial. Methods. We assessed the nature and severity of anginal symptoms and the use of antianginal and anti-ischemic interventions before enrollment in the 1842 men and 389 women with left ventricular ejection fractions ≤40 percent after an acute myocardial infarction who were randomized in the Survival and Ventricular Enlargement trial. Results. Before their index infarction, women were as likely as men to have had angina and to have been treated with antianginal drugs. However, despite reports by women of symptoms consistent with greater functional disability from angina, fewer women had undergone cardiac catheterizati...

Background Atrial arrhythmias (AA) affect up to 40% of patients following cardiac surgery. The best strategy for prevention of AA remains undetermined, however, beta blocker (BB) administration is the standard of care at many centers (including ours). Although there is now compelling evidence demonstrating the utility of magnesium sulphate (MgSO4) for treatment of AA, the effectiveness of MgSO4 for prophylaxis of AA remains controversial. This study is the largest randomized, placebo-controlled trial of intravenous (IV) MgSO4 for the prevention of AA following cardiac surgery. Methods Eligible patients requiring either coronary artery bypass graft surgery (CABG), or valve surgery ± CABG, were randomized to receive either 5g IV MgSO4, or placebo upon removal of the crossclamp, followed by daily infusions of IV MgSO4 or placebo over 4 hours, from the day of surgery until post-operative day 4. All patients were treated according to an established protocol with oral BB (atenolol). Patients were monitored by continuous telemetry for the first 5 post-operative days. The primary endpoint was an AA lasting ≥ 30 minutes, or requiring treatment because of hemodynamic compromise. Results Table 1 summarizes the results. There was no difference in the incidence of AA between patients who received IV MgSO4 or those who received placebo. Conclusions In patients proactively treated with atenolol using an established protocol, the addition of daily IV MgSO4 infusions for 5 days post-operatively did not reduce the incidence of clinically important AA following cardiac surgery. Results For Primary Outcome (Post-Operative AA)

We report a case of 63-year-old man who developed massive pulmonary hemorrhage following intravenous streptokinase for acute myocardial infarction. Pulmonary hemorrhage was diagnosed by the triad of hemoptysis, a drop in hematocrit, and a new unilateral infiltrate on chest radiograph. This diagnosis was confirmed by autopsy findings. Pulmonary hemorrhage has rarely been reported following thrombolytic therapy. We believe that pulmonary hemorrhage is a rare but a potentially life-threatening complication of thrombolytic therapy and should be considered in the differential diagnosis of pulmonary infiltrates or falling hemoglobin after thrombolytic therapy for acute myocardial infarction with no obvious site of bleeding.

Objectives We evaluated the effects of long-term therapy with the angiotensin-converting enzyme (ACE) inhibitor ramipril on major cardiovascular (CV) outcomes in high-risk women. Background The effect of long-term ACE inhibitor therapy in high-risk women without heart failure and with preserved left ventricular (LV) systolic function has not been previously reported. Methods The Heart Outcomes Prevention Evaluation (HOPE) trial is a large, randomized clinical trial that evaluated ramipril and vitamin E in high-risk patients. We present the preplanned analysis of the effects of ramipril in women in the HOPE study. The study randomized 2,480 women aged ≥55 years with vascular disease or diabetes and at least one additional CV risk factor and without heart failure or a known low LV ejection fraction to ramipril (10 mg/day) or placebo. The primary outcome was the composite of myocardial infarction, stroke or CV death. Average follow-up was 4.5 years. Results Treatment with ramipril resulted in reduced primary end point rates (11.3% vs. 14.9% in the placebo arm; relative risk [RR] 0.77, 95% confidence interval [CI] 0.62 to 0.96; p = 0.019), fewer strokes (3.1% vs. 4.8%; RR 0.64, 95% CI 0.43 to 0.96; p = 0.029) and fewer CV deaths (4.2% vs. 6.9%; RR 0.62, 95% CI 0.44 to 0.88; p = 0.0068). There were trends toward reduced rates of myocardial infarction, heart failure and all-cause death. The beneficial effect of ramipril was similar in women and men. Conclusions Treatment with ramipril reduces the CV risk in high-risk women without heart failure and with preserved LV systolic function.

Objectives. This study was conducted to evaluate the degree of neurohumoral activation around the time of hospital discharge after myocardial infarction. Background. Because pharmacologic interventions that block the effects of neurohumoral activation improve the prognosis after infarction, we hypothesized that widespread neurohumoral activation persists in some patients until at least the time of hospital discharge and that the determinants of activation vary from one system to another. Methods. Five hundred nineteen patients in the Survival and Ventricular Enlargement Study (SAVE) had plasma neurohormones measured before randomization at a mean of 12 days after infarction. All patients had left ventricular dysfunction (left ventricular ejection fraction ≤40%) but no overt heart failure. Results. Although all neurohormones except epinephrine were increased compared with values in age-matched control subjects, plasma norepinephrine (301 ± 193 vs. 222 ± 87 pg/ml, p < 0.001), renin activity (3.0 ± 3.7 vs. 1.2 ± 1.2 ng/ml per h, p < 0.001), arginine vasopressin (1.9 ± 6.9 vs. 0.7 ± 0.3 pg/ml, p < 0.001) and atrial natriuretic peptide (75 ± 75 vs. 21 ± 9 pg/ml, p < 0.001) values ranged from normal to very high, indicating a wide spectrum of neurohumoral activation. Activation of one system did not correlate with activation of another. The clinical and laboratory variables most closely associated with neurohumoral activation were Killip class, left ventricular ejection fraction, age and use of diuretic drugs. The association between neurohumoral activation and clinical and laboratory variables varied from one neurohormone to another. Conclusions. Neurohumoral activation occurs in a significant proportion of patients at the time of hospital discharge after infarction. Which neurohormone is activated and which clinical and laboratory variables determine this activation vary from one neurohormone to another.

Previous studies have indicated that patients with an acute myocardial infarction have marked activation of all neurohumoral systems on admission to the hospital. This activation begins to subside within the first 72 hours so that by 7-10 days, all plasma neurohormones have returned to normal. The only documented exceptions were found to occur in patients with left ventricular dysfunction and overt heart failure, where both plasma renin activity and atrial natriuretic peptide were increased, and in patients with left ventricular dysfunction but no overt heart failure, where only atrial natriuretic peptide was increased. Although these studies suggest that neurohumoral activation rarely occurs at the time of hospital discharge, they were small and may have missed an important subgroup of patients with persistent neurohumoral activation. In the Survival and Ventricular Enlargement (SAVE) study, 522 patients had plasma neurohumoral levels measured at a mean of 12 days postinfarction. All SAVE patients had left ventricular dysfunction (left ventricular ejection fraction less than or equal to 40%), but no overt heart failure. In this group of patients, all neurohumoral levels (plasma renin activity, norepinephrine, arginine vasopressin, and atrial natriuretic peptide) were found to be increased compared with age-matched control subjects. These results indicate that, in fact, a subgroup of patients without overt heart failure has persistent neurohumoral activation at the time of hospital discharge postinfarction, and that this activation involves several neurohumoral systems. Since patients with persistent neurohumoral activation postinfarction are likely those most at risk of developing complications and the ones most likely to benefit from pharmacologic interventions blunting the effects of neurohumoral activation, measurement of predischarge neurohumoral levels may be useful.

It has been found that by carrying out simple modifications to the Manley ventilator, consisting of an extra weight and an adjustable safety valve an improvement in the versatility and safety of the ventilator is accomplished.

140 consecutive patients undergoing selective coronary angiography in the investigation of chest pain had fasting blood specimens collected. 24 specimens were unsuitable due to hemolysis or to incomplete coronary angiography studies. In the 116 remaining patients the serum was analyzed for total cholesterol, free cholesterol, and the initial rate of cholesterol esterification. LCAT activity was determined both as the percentage esterification per minute, and as nmols/ml/min. All the coronary angiograms were examined by a single cardiologist who was unaware of the results of the serum tests. Fixed predetermined criteria were used, resulting in all patients being classified as one of four groups. 36 patients had no detectable atheroma, 23 mild, 21 moderate, and 36 severe. Statistical analysis revealed a significant relationship between the presence and severity of coronary atheroma with the patient's age, and an equally strong relationship was found with the patient's total serum cholesterol. No statistically valid correlation could be found between LCAT activity (as determined by esterification in the patient's native serum) and atheroma. Free cholesterol levels also did not correlate with the presence of antheroma. An interesting finding was the presence of severe antheroma in a small number of patients with low normal level of serum cholesterol and high LCAT activity.

Thirty-six patients with chronic, stable angina pectoris were studied during 2-week treatment periods in which they received, in a randomized double-blind, crossover study, a new calcium entry blocking agent, isradipine, 7.5 mg three times daily or placebo. Antianginal efficacy was determined by treadmill exercise testing carried out 3 and 9 hours after drug administration on the final day of each treatment period. During placebo therapy, treadmill exercise time to the onset of angina (P1) and to the development of moderate angina (P2) was similar at 3 and 9 hours and similar to the placebo run-in period. During isradipine therapy, treadmill exercise time 3 hours after dosing was greater than with placebo therapy (P1 312 +/- 23.0 vs. 267 +/- 19.5 seconds, p less than 0.001; P2 410 +/- 20.2 vs. 355 +/- 18.8 seconds, p less than 0.002). Nine hours after drug administration, the results of exercise testing were similar to placebo.

The initial fractional rates of cholesterol esterification were measured in human cord serum, in a group of apparently healthy “young adults” (mean age ± S.D. 32 ± 5 years), in a group of “middle aged” adults (51 ± 8 years) with normal coronary angiograms and in newborn, 10-, 20-, 45-, 180- and 365-day-old rats. The initial fractional rate of esterification was inversely related to serum cholesterol levels in humans and, with the exception of newborns, also in rats. A theory of lecithin: cholesterol acyltransferase participation in cholesterol metabolism is discussed.

Two hundred milligrams of lidocaine hydrochloride was given intramuscularly for controlling ventricular premature beats in 40 patients continuously monitored in an intensive care unit. In 14 patients, serum levels were determined by gas chromatographic technique. The treatment abolished premature ventricular beats in 30 of the 40 patients. Eight of the failures had persistent premature ventricular beats over a long period before admission to hospital. Serum levels and clinical results showed that effective drug concentrations were reached between 15 to 30 minutes after injection and that therapeutic levels were maintained for at least 60 minutes. It is suggested that lidocaine should be given intramuscularly to patients suffering an acute myocardial infarction before they are moved to hospital to prevent serious ventricular arrhythmias during the prehospital phase.