Determining prognosis after acute myocardial infarction in the thrombolytic era
BMJ 1998; 316 doi: https://doi.org/10.1136/bmj.316.7134.865a (Published 14 March 1998) Cite this as: BMJ 1998;316:865
Rescue angioplasty after failed thrombolysis may put patients at risk
- Pitt Lim, Clinical lecturer,
- Paul Shiels, Research fellow
- Department of Clinical Pharmacology and Cardiology, Ninewells Hospital and Medical School, Dundee DD1 9SY
- Cardiovascular Division, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA
EDITOR—Beller brings to readers' attention the fact that routine invasive procedures after acute myocardial infarction offer no significant benefit over that offered by the routine practice of risk stratification with non-invasive methods.1 We are concerned, however, with the blanket statement that high risk patients should have early angioplasty or rescue angioplasty after failed thrombolysis. This technique should be used with caution.
A meta-analysis by Ellis et al indicated a mortality of 10.6% after the procedure, either from the disease process or as a direct complication of the procedure.2 Furthermore, this procedure fails in 20% of cases and those failed cases have a mortality of 40%. Vigorous clinical assessment is therefore necessary before a patient is classified as being at high risk. Inadequate optimisation of supportive treatment often leads to signs such as hypotension and sinus tachycardia, which in turn predispose to further chest pain, interpreted as postinfarction angina even in the absence of electrocardiographic changes. Chest crepitations related to aging are often confused with those associated with pulmonary oedema. One prime example is inferior myocardial infarction with right ventricular extension. This is due to an occlusion of a dominant right coronary artery, which carries a relatively good prognosis. Suboptimal fluid replacement and the indiscriminate use of inotropic agents without prior careful assessment of left ventricular function with echocardiography and guidance by Swan-Ganz catheterisation lead to patients being classified as at high risk without having prior or incidental left coronary artery disease.
The fact that rescue angioplasty for right coronary artery occlusion is associated with excessive complications3 should lead doctors to question whether this form of intervention is putting a patient's life at risk, turning a relatively benign course into a fatal one.
References
Author's reply
- George A Beller, Chief
- Department of Clinical Pharmacology and Cardiology, Ninewells Hospital and Medical School, Dundee DD1 9SY
- Cardiovascular Division, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA
EDITOR—Lim and Shiels make a valid point regarding the increased risk of rescue angioplasty after presumed failed thrombolysis, but I never addressed the issue of early angioplasty in my editorial. The thrust of my discussion regarding risk stratification related to the identification of clinical variables and variables determined with non-invasive tests that could be used to select those patients after infarction who are most likely to benefit from coronary angiography and coronary revascularisation.
With respect to clinical variables, I mentioned that the combination of rales in over a third of the lung field, hypotension, and sinus tachycardia on admission was an important observation that indicated a high risk status, since these haemodynamic alterations reflect a large area of myocardium at jeopardy with ischaemia or necrosis, or both; they can also point to underlying multivessel disease or a large infarct, or both. I agree that each one of these haemodynamic changes in isolation is not highly specific for a high risk designation. Certainly, crackles at the lung bases alone without evidence of other signs of left ventricular pump failure can indicate atelectasis or pulmonary disease. Hypotension in isolation, without sinus tachycardia and pulmonary rales, can be due to volume depletion or right ventricular infarction and not be secondary to extensive left ventricular dysfunction.
The main message of my editorial was that a routine invasive strategy for risk assessment before discharge is not superior to a watchful waiting, non-invasive strategy in which patients undergo angiography for high risk clinical findings or for spontaneous or inducible ischaemia within or remote from the infarct zone. Recent data reported from the VA non-Q wave infarction strategies in-hospital trial, in which 920 patients with non-Q wave infarction were randomised to an initial invasive strategy or an initial conservative strategy, support this approach.1 At one year after discharge there was no difference in cardiac death or recurrent infarction between the two groups. Also, new data from Yusuf et al showed no difference in outcome for patients with infarction admitted to hospitals with cardiac catheterisation facilities (catheterisation rate 66%) compared with those admitted to hospitals with no catheterisation facilities on site (catheterisation rate 34%).2