© 2004 European Society of Cardiology
Acute coronary syndromes presenting solely with heart failure symptoms: are they under recognised?
University Department of Medicine City Hospital, Birmingham B18 7QH, UK
* Corresponding author. Tel.: +44-121-507-4476/5634; fax: +44-121-554-4083. E-mail address: robert.macfadyen{at}swbh.nhs.uk
Key Words: Chest pain symptoms • Breathlessness • Heart failure • Angina equivalent • Mechanical coronary interventions • Risk benefit ratio
Received June 27, 2003; Revised February 9, 2004; Accepted February 25, 2004
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1. How often do we recognise breathlessness as a presenting symptom of ischaemia? |
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 Top 1. How often do... 2. Are symptoms suggestive...3. Practical considerations in...4. Identifying acute heart...5. ConclusionReferences |
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In acute coronary syndromes (ACS), the difference between myocardial (reversible) ischaemia and (irreversible) infarction can often be due to either a delay in presentation from the onset of symptoms and the timing and efficacy of any administered treatment. Whilst current guidelines promote aggressive coronary revascularisation for troponin positive unstable angina (UA) or Non-ST elevation MI (NSTEMI), most patients who fall into this category are identified by their recurrent or worsening chest pain symptoms [1]. What is often forgotten is that myocardial ischaemia can also be identified by the development of classical heart failure-type symptoms, including breathlessness at rest or signs of left ventricular systolic dysfunction (S3 gallop, radiographic pulmonary oedema, or rarely, new or worsening mitral regurgitation (MR)).
Where the signs or symptoms of heart failure predominate with little or no complaints of chest pain, some cases of potentially reversible ischaemia will be labelled non-specifically as ‘acute heart failure’. While some expert cardiologists suggest that this is ‘common knowledge’, there are no reliable estimates of how many acute heart failure patients have symptoms mainly due to reversible ischaemia rather than irreversible infarction or an acute presentation of chronic heart failure.
This distinction is important in the first 24 h following presentation, as it is likely that many such patients are not managed in cardiac units but in high dependency emergency medical admission areas. If revascularisation is a priority, there may be a potentially large number of ACS patients presenting with heart failure that will be left unrecognised or untreated. Early identification of this sub-group of patients is important if potentially reversible myocardial ischaemia is to be identified and managed by revascularisation.
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2. Are symptoms suggestive of systolic failure an ominous accompaniment of ACS? |
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Left ventricular ejection fraction is a long established independent predictor of cardiovascular mortality, both in chronic heart failure and/or following myocardial infarction [2–4]. Certainly, the appearance of heart failure-type symptoms accompanies a poorer prognosis in ACS and often accompanies more severe coronary disease [5,6].
The occurrence of heart failure symptoms at some point among ACS presentations is also common (26% in the EuroHeart dataset), and is associated with increased in-hospital and 30-day mortality (with or without the presence of left ventricular systolic dysfunction (LVSD)). The latter emphasis is important given recent information that acute heart failure symptoms with preserved systolic function still carries a significant mortality risk [7], albeit less than symptomatic presentations of left ventricular systolic dysfunction.
In a recent report from the Global Registry of Acute Coronary Events (GRACE) observational registry, the presence of heart failure-type symptoms was also associated with reduced hospital and 6-month survival across all ACS subsets, including patients with normal markers of necrosis [8]. Importantly, GRACE was a large prospective registry of 16 166 patients hospitalised with ACS, which identified 13 707 patients without prior HF or cardiogenic shock at presentation-of these, 1778 (13%) had an admission diagnosis of HF (Killip class II or III) and this was associated with a marked increase in mortality rates during hospitalisation (12.0% vs. 2.9% without HF, P<0.0001) and at 6 months after discharge (8.5% vs. 2.8%, P<0.0001). By logistic regression analysis, admission HF was an independent predictor of hospital death (odds ratio, 2.2; P<0.0001), as well as of longer hospital stay and higher readmission rates. Furthermore, patients with HF had lower rates of catheterisation and percutaneous cardiac intervention, and fewer received beta-blockers and statins.
Similarly, heart failure complicating ACS in the SHOCK Trial Registry [9] had similar in-hospital mortality to heart failure complicating completed acute myocardial infarction. The SHOCK Trial Registry also demonstrated that prognosis in these patients was improved if coronary intervention/revascularisation was executed speedily [10,11]. As in the GRACE registry, ACS patients with heart failure who had in-hospital revascularization had significantly lower 6-month death rates (14.0% vs. 23.7%, P<0.0001; adjusted hazard ratio, 0.5; 95% CI, 0.37 to 0.68, P<0.0001) [8].
Despite these data, ACS patients presenting with heart failure in current clinical practice are less likely to undergo invasive investigation with a view to revascularisation. Unfortunately, outcomes (death, reinfarction, revascularisation and hospitalisation) in cardiac emergencies are time dependent, and delays in establishing ischaemia as the cause of heart failure symptoms in ACS patients can be made worse by a further delay in, or deferred treatment. Such delays may result allowing the potential emergence of cardiogenic shock can mask any treatment benefit in the critically ill, as outcome data from the SHOCK Trial Registry has convincingly demonstrated [12].
Factors thought to contribute to a reluctance or a delay in performing coronary angiography include concomitant co-morbidity, the practical problems associated with coronary angiography in a patient with acute pulmonary oedema, or simply ‘old age’. One potential pitfall in clinical trials or surveys/observational studies of presentations of ACS (and the subsequent endpoint analyses) is the exclusion of ‘shocked patients’ (often including those in acute pulmonary oedema or with impending/established cardiogenic shock). By excluding such patients endpoint data in many publications are both inaccurate and fail to address the potential benefit of intervention such patients could gain.
Thus, further clinical studies are required to assess what proportion of patients presenting solely with HFS (without chest pain) have an acute ischaemic (and potentially reversible) aetiology as the causative factor for their presentation, as much more aggressive treatment of these patients may be warranted to improve prognosis.
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3. Practical considerations in the management of ACS patients presenting with heart failure |
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Top1. How often do...2. Are symptoms suggestive...3. Practical considerations in...4. Identifying acute heart...5. ConclusionReferences |
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Patient selection amongst presentations of ACS will invariably affect outcome. For example, the PRIMA study found a lower 1-year mortality in myocardial infarction patients referred for immediate angiography (6.5% for the coronary angiography group vs. 36.9% for non-coronary angiography group) [13]. Patients with a poor symptomatic state at initial presentation, as reflected by Killip class III or IV on admission, had a much higher 1-year mortality; however, these patients did not undergo an early interventional strategy, and it remains inconclusive whether they would have benefited from early angiography and/or revascularisation [13]. Thus, some selection bias may operate with invasive investigations and revascularisations being performed mostly in those at lowest risk who do well with (and possibly without) coronary interventions. This seeks to reinforce a conservative practice when dealing with patients presenting with ACS with no clear guidance on the potential benefits to be gained by treating those at highest risk and potentially the most benefit to gain.
Given current advances in percutaneous coronary interventions, better access to coronary bypass surgery and better peri-procedural drug management, as well as the increasing use of percutaneous revascularisations even in diffuse or severe CAD (something commonplace in ACS with HFS), there should be more consideration towards revascularisation in these high risk patients. These high risk patients should have unrestricted triage, easy and rapid access to diagnostic angiography with subsequent rapid referral for revascularisation where feasible. This approach applies to patients with acute myocardial infarction, ACS [14] and even patients with cardiogenic shock. Such a strategy will be more complex in older patients with more complex coronary lesions and perhaps with increased peri-procedural mortality, but the key issue is in identifying the patient and acting early. Why should such a strategy not be adopted in ACS presentations of heart failure symptoms with or without overt chest pain where ischaemia is the cause of the acute failure? In many centres in the United Kingdom, for example, such delays can result from the limited involvement of cardiologists in unselected acute medical admissions where little other than chest pain cases may be seen acutely. Indeed, it is likely that many cardiologists will not see these patients, as they often do not survive to be referred 24–48 h after admission to general medical teams.
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4. Identifying acute heart failure for revascularisation |
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Top1. How often do...2. Are symptoms suggestive...3. Practical considerations in...4. Identifying acute heart...5. ConclusionReferences |
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Simple symptomatic severity such as the Killip classification applied to patients admitted following a myocardial infarction [15] is an accepted early prognostic marker [16]. This has been supplanted by more technical methods such as echocardiographic wall motion scores [17] or myocardial contrast echocardiography [18]. Early studies on the impact of invasive coronary procedures on survival after myocardial infarction have shown benefit for those patients in classes II and III undergoing cardiac catheterisation and revascularisation within 30 days of admission, whereas those patients in Killip class I were least likely to benefit [19].
Thus, targeting the most severely affected patients derives the most benefit, but the application of technical assessments or clinical risk scoring alone does not seem enough. For example, in the two-thirds of patients in the EuroHeart survey who had an ejection fraction measured, those with reduced ejection fraction were paradoxically less likely to undergo cardiac catheterisation despite having increased mortality.
Given that symptoms and signs alone are a non-sensitive indicator of the likelihood that presentations of heart failure symptoms have an underlying acute ischaemic aetiology, can current sensitive biochemical markers help the triage of such patients? Troponin measurements, while still affected by issues of non-specificity, are exquisitely sensitive and will identify ischaemic patients at high risk of death. Minor acute troponin release (in the absence of significant release of CK or CKMB) also defines a ‘high risk’ group of heart failure presentations [20]. Despite the value of this measure in conventional chest pain presentations, it is still unclear whether these may indicate a need to proceed with angiography and or revascularisation in a heart failure presentation. Instead, the TACTICS TIMI 18 study has shown that BNP levels (a marker of ventricular impairment even in this setting) highlights ‘high risk’ ACS patients affected by ischaemia who can benefit from coronary interventions over and above those defined by troponin [21]. However, troponin release [22] will not discriminate between an ischaemic insult and non-ischaemic heart failure [23].
We suggest that the combination of the following would help triage ACS patients presenting with heart failure symptoms (Fig. 1): (i) Clinical symptoms and signs of cardiac failure; (ii) appropriate biochemical markers (possibly troponin or BNP); (iii) an ECG during symptoms, and (iv) possibly echocardiography to define wall motion abnormalities could provide a better combination of indicators for early stratification and intervention for appropriate high-risk patients. Ultimately we need to recognise the ischaemic aetiology, define it and, most importantly, act quickly to facilitate relief of ischaemia, possibly by a revascularisation procedure.
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5. Conclusion |
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Prompt effective and comprehensive reperfusion is accepted best practice for patients with a recognised ACS. Equally prompt and aggressive mechanical reperfusion may have a role in some patients with cardiogenic shock secondary to acute ischaemia. Although there are little supportive data, one can presume there are a number of ACS patients with reversible who present with predominant breathlessness and who are non-specifically labelled as ‘acute heart failure’. Their treatment based on medical measures for heart failure (diuretics, ACE inhibition and possibly inotropic support) is likely to be sub optimal, largely due to failure to recognise and treat ischaemia as an aetiology, rather than a clinical presentation of heart failure symptoms.
Identifying patients for appropriate treatment will include seeking reversible ischaemia by careful history, and combining this with appropriate testing and defining ischaemia from infarction or contractile failure secondary to other causes. Nonetheless, we also need to know whether or not revascularisation is of benefit in this group of patients. A similar question is now being asked of surgical revascularisation for chronic ischaemic cardiomyopathy in the HEART-UK trial [24]; we urgently need the same answers in ACS patients presenting predominantly as heart failure symptoms.
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