findings on coronary angiography; type 2 MI causes, such as elevated LVEDP and severe hypertension, are re-examined.
When ischemic imbalance occurs without underlying CAD, troponin I usually remains <0.5–1 ng/ml.6-8 However, when ischemic imbalance occurs on top of underlying stable CAD, troponin I may rise to levels >1 ng/ml. Therefore, a troponin I level >1 ng/ml suggests obstructive CAD, whether the primary insult is coronary (thrombotic, type 1 MI) or non-coronary (type 2 MI); the positive predictive value for CAD is high and approaches 90%, less so if renal dysfunction is present.6 Conversely, any degree of troponin rise, even if very mild (e.g., 0.04 ng/ml), in a patient with angina and without a context of secondary ischemia indicates type 1 MI until proven otherwise on angiography.
In a type 2 MI setting, aside from the degree of troponin rise (>1 ng/ml), pronounced angina, pronounced ST abnormality on the ECG, or wall motion abnormality signals underlying CAD and may compel a consideration of type 1 MI.
Acute bleed, severe anemia, or tachyarrhythmia destabilizes a stable angina. Treating the anemia or the arrhythmia is a first priority in these patients, taking precedence over treating CAD.
Acute HF often leads to troponin elevation because of microcirculatory compression by the high LVEDP and because of direct cardiomyocyte injury from wall stretch and neurohormones. Troponin may even rise to >1 ng/ml in 6% of patients regardless of any underlying CAD.9 Thus, an elevated troponin, by itself, does not establish the diagnosis of ACS in a patient presenting with HF.1 In fact, most troponin elevations in HF are not even type 2 MI, but rather “non-MI troponin elevation”. Yet, if CAD has not been addressed previously, coronary angiography is still warranted to address the underlying etiology of HF, after diuresis and preferably before discharge, with early revascularization if appropriate.
Conversely, acute HF with ischemic ST changes, new Q waves, severe troponin rise, or new segmental akinesis may be considered type 1 MI and treated as such, unless CAD has been ruled out recently. About 30% of acute HF presentations are triggered by ischemia.10
In acute HF, chest tightness is frequently a description of dyspnea and does not equate with CAD. Crescendo exertional chest discomfort that precedes HF is more suggestive of CAD.
While acute severe hypertension may cause type 2 MI, it may also result from type 1 MI with severe angina (catecholamine surge). In type 1 MI, hypertension drastically improves with angina relief and nitroglycerin, whereas in malignant hypertension, hypertension is persistent and difficult to control despite multiple antihypertensive therapies, nitroglycerin only having a minor effect. Nitroglycerin has a mild and transient antihypertensive effect, and thus a sustained drop in BP with nitroglycerin often implies that hypertension was secondary to MI.
Management of type 2 MI- The primary therapy is directed towards the primary insult (e.g., sepsis, anemia, severe HTN, tachyarrhythmia). Acute antithrombotic therapy and coronary angiography are not warranted. Ischemic work-up, by means of stress testing or coronary angiography, is electively performed, before or after discharge.
For example, in a patient with gastrointestinal (GI) bleed and angina, the primary treatment consists of transfusion and GI therapy, e.g., endoscopic cauterization. Antithrombotic drugs should be avoided for at least few days, and, if possible, weeks. Depending on the ECG, the echo findings, and the severity of anemia, coronary angiography may not be required. For example, a mild troponin rise of 0.3 ng/ml without significant ECG abnormalities, occurring with acute and severe anemia, may not require coronary angiography. On the other hand, troponin rise with a nadir hemoglobin of 8–10 mg/dl and with ST changes often requires coronary angiography.
Importance of differentiating the two subtypes of type 2 MI- A large European registry distinguished between type 2 MI with underlying CAD (CAD history or new CAD diagnosis during admission), and type 2 MI without underlying CAD.8 Half of patients with type 2 MI had no underlying CAD. In type 2 MI without CAD, troponin was <0.6 ng/ml, whereas with underlying CAD it could exceed 1 ng/ml. From a cardiovascular standpoint, the prognosis was impressively benign in patients with type 2 MI without underlying CAD, whose mean age was 72: no cardiac mortality and 0.8% overall mortality at 3 months. Conversely, patients with type 2 MI and underlying CAD had a cardiac mortality comparable to type 1 MI at 3 months (~4% vs. 5%), and an overall mortality higher than type 1 MI (9 vs 6%) (higher mortality related to older age [mean age 76], more comorbidities and higher BNP). Similar observations were made in other registries, except for the finding of a high non-cardiac mortality in all type 2 MIs.11,12
Thus, while the acute management of type 2 MI is the same regardless of underlying CAD, long-term management is dramatically different when underlying CAD is present and somewhat resembles the long-term management of type 1 MI (Table 1.1 ).
Table 1.1 Tips in MI definition
| In the absence of clinical or ECG features of MI, the troponin rise is not even called MI (called injury).Most troponin elevations in HF are not even type 2 MI, but rather “non-MI troponin elevation”The term NSTEMI is reserved for type 1 MI. Type 2 MI is not called “type 2 NSTEMI”Type 2 MI with underlying CAD is managed differently than type 1 MI (no antithrombotic therapy, no acute revascularization). Yet, from the standpoints of cardiac prognosis and chronic management, type 2 MI with CAD is somewhat comparable to type 1 MI and dramatically different than type 2 MI with no CAD, which has a much better prognosis. This suggests the importance of eventual CAD work-up after type 2 MI.A case may initially be considered type 1 MI, only to be later reconsidered type 2 MI once evidence of an acute noncardiac illness arises (e.g., fever, bacteremia) or once coronary angiography shows no acute disease. The reverse may also be true.ST depression is common during fast tachyarrhythmias and after their conversion to sinus rhythm (cardiac memory), even in the absence of ischemia. It is not specific for MI definition in this setting. |
C. Non-ischemic myocardial injury (also called “non-MI troponin elevation”)
In this case, myocardial injury occurs because of a demand-supply imbalance similar to type 2 MI but less profound and with less CAD, or because of a direct cardiomyocyte injury (trauma, myocarditis, rhabdomyolysis, cytokines and neurohormones in shock, stroke, or post-operative states). This injury may be chronic with steady, chronic troponin elevation (e.g., advanced kidney disease or cardiomyopathy).*
Therapy is directed towards the primary insult. The cardiac prognosis depends on the presence of CAD and is generally better than type 2 MI, as CAD is less likely.10
D .Coronary vasospasm and microvascular dysfunction
It was initially hypothesized by Prinzmetal and then demonstrated in a large series that coronary vasospasm and vasospastic angina most often occur in patients with significant CAD at the site of a significant and sometimes unstable atherosclerotic obstruction.13-15 In fact, a ruptured plaque is commonly accompanied by vasospasm, as the activated platelets and leukocytes release vasoconstrictors.
Vasospasm also frequently occurs without obstructive coronary atherosclerosis and may lead to chronic vasospastic angina. In fact, in the current era, the term “coronary vasospasm” is mainly used to identify this “isolated coronary vasospasm” with no severe CAD. Indeed, isolated vasospasm is frequently the underlying disease process in patients with typical angina or MI yet no significant CAD.16-19 The diagnosis
