Not all heart attacks are created equal. The type of heart attack can influence the prognosis greatly. A heart attack can be recognized by clinical features of chest pain or shortness of breath, ECG or cardiac imaging findings and elevated biochemical markers including the cardiac troponin, the so-called “heart attack blood test”.
The development of ever more sensitive and heart tissue specific cardiac bio markers and more sensitive imaging techniques now allows for detection of very small amount of heart damage or myocardial necrosis. The use of high sensitive troponin assays (used in Europe but not yet in the US) allows for the detection of low levels of troponin even in normal healthy subjects. The majority of cardiac troponin is inside the cardiac cell. The release of cardiac troponin into the bloodstream can involve several mechanisms including cell necrosis, formation of blebs or leakage of the cardiac cell membrane or release of enzymes that can break down troponin. Sometimes rapid heartbeat (tachycardia) or transient myocardial ischemia (angina) can release intact cardiac troponin into the blood.
It is recognized that in the presence of the clinical history suggestive of acute coronary syndrome and ECG abnormality, an elevated troponin result greater than the 99th percentile compared to a reference group is indicative of myocardial necrosis. However, what is more important is those serial troponin measurements can help establish whether the patient’s chest pain is of cardiac origin and whether the patient is having a true myocardial infarction. The patients presenting in the emergency room with chest pain do not all have a myocardial infarction. A higher sensitivity troponin test can help differentiate earlier and more accurately whether the patient is having a myocardial infarction or not. Consequently, serial negative troponin tests have a very good predictive value attesting that these patients can be discharged safely and have a good outcome post discharge. The troponin measurements must be interpreted in the context of the probability of coronary artery disease.
Our 1st patient is a 65-year-old male with diabetes and hyperlipidemia who presented with increasing frequency of chest pain and shortness of breath. His 1st troponin was normal at 0.03 ng/ml. His repeated troponin was only slightly elevated at 0.056ng/ml. He was still having some chest discomfort and he was taken to the cardiac catheterization lab where a severe stenosis of the proximal right coronary artery was recognized and treated with coronary stenting.
Not all heart attacks are created equal.
Because of the new techniques for detection of MI and the ever evolving treatment of MI, the WHO (World Health Organization) has been updating the universal definition and classification of MI recognizing the diverse conditions that cause a heart attack. The diagnosis of MI requires evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia. It requires the detection of a RISE and/ or FALL in cardiac troponin with at least one value above the 99th percentile upper reference limit AND at least one of the following: 1) symptoms of myocardial ischemia (chest pain, shortness of breath…), 2) new ECG changes (st segment or LBBB) or development of a Q wave, 3) imaging evidence of MI or new wall motion abnormality (MRI, echo or nuclear), 4) a clot or thrombus by angiogram. Understanding that different types of MI are treated differently, 5 types of MI have been recognized.
Not all heart attacks are created equal: Type 1 MI
A type 1 MI is a spontaneous MI caused by an atherosclerotic plaque rupture, ulceration, fissuring, erosion or dissection resulting in a formation of clot or thrombus in the coronary artery resulting in the decrease myocardial blood flow and myocardial necrosis. The patient may have underlying severe CAD but on occasion the atherosclerosis can be minimal. These patients can present as STEMI or Non-STEMI. Over the years, treatment with percutanous coronary intervention has been demonstrated to be the best treatment option for these patients. In addition, secondary prevention with anti-platelet therapy and cholesterol treatment has demonstrated significant improvement in the outcome of these patients.
Our next patient is a 61 yo male who developped severe restrosternal chest pain while eating breakfast. The pain persisted all day and he presented to the ER with an ECG showing a right bundle branch block (RBBB) and anterior ST segment elevation (STEMI). Cardiac catheterization revealed a total occlusion of his proximal LAD or widow maker.
The next patient suffered a non-STEMI. She is a 64 yo women with uncontrolled HTN, hyperlipidemia and diabetes mellitus. She presented with intermittent left sided chest tightness radiating to the left arm, accompanied by sweating and extreme weakness. She had several episodes in the last month and, on the morning of admission, she had a 30 minute episode that was more severe than before. In the ER, her ECG showed ST segment depression and her initial troponin measured 0.11 ng/ml. The troponin peaked at 1.99 ng/ml and the angiogram showed critical stenosis of the LAD.
Not all heart attacks are created equal: Type 2 MI
A type 2 MI is usually caused by an imbalance between supply and demand. It compromises a diverse group of heart attack patients who have myocardial ischemia secondary to a variety of acute medical or surgical conditions. In these cases, myocardial injury occurs when the myocardial oxygen supply is decreased i.e. severe hypoxemia caused by respiratory failure, severe hypotension, coronary spasm, coronary embolism (below). This patient is a 32 yo men with a past history of hypertrophic non-obstructive cardiomyopathy, ventricular tachycardia s/p dual ICD pacemaker and severe diastolic heart failure. He presented with mid-sternal chest pain, profuse sweating and severe shortness of breath. A coronary arteriogram 6 months prior showed normal coronaries. His troponin was 3.99 ng/ml and the repeated arteriogram showed total and abrupt occlusion of the marginal branch of the circumflex artery.
The echo demonstrated a clot at the apex of the LV. This was felt to be the source of the coronary embolization and the resulting type 2 MI.
Or when demand exceeds supply with some such condition as tachycardia such as this patient with newly diagnosed atrial fibrillation and rapid ventricular response (approximately 150 beats per min):
Other patients may have severe hypertension with/without LVH m (LV hypertrophy), severe blood loss anemia or stress (Takotsubo). As an examble this is a 63 yo women who received the very devastating and unexpected news that her brother had died from an accident. Two hours later she developed chest pain and presented to the ER with ECG changes compatible with an anterior STEMI and troponin elevated at 5 ng/ml. Her arteriogram showed normal coronary arteries and akinesis of the distal anterior and inferior walls (below).
Type 2 MIs can happen in patients without coronary artery disease. Currently there is no guidance or consensus on the optimal cardiac investigation, management or treatment strategy for patients. Clinically, one of the main issues is to determine whether the patient had a heart attack at all. Patients admitted to the hospital with all kinds of symptoms get a troponin drawn for different reasons. It should be recognized that patients with advanced age and patients with chronic renal failure, on dialysis, can have chronic myocardial ischemia and chronically elevated troponin. Even if the clinical probability of underlying CAD is high, a final diagnosis of type 2 MI requires the demonstration of a changing troponin value. This is the best way to distinguish between acute or chronic myocardial injury. The 2nd step is to differentiate whether the troponin elevation is reflecting an actual MI versus one that is caused by another reason. A troponin rise with chest pain and new ECG changes usually indicates an AMI. Other causes of troponin rise such as massive or sub-massive pulmonary emboli, pneumonia or myocarditis should prompt the treatment of the primary disease. A troponin rise in these conditions usually indicates an adverse clinical outcome. Where coronary artery disease is identified, the clinical outcome could be improved with revascularization or medical therapy.
Not all heart attacks are created equal: Type 3 MI
A type 3 MI includes cardiac death with symptoms suggestive of myocardial ischemia prior to the death and that presents to the emergency room with new ECG changes including left bundle branch block.
Our patient is a 60-year-old woman with hypertension and smoking history who presented to an outside hospital with back pain and chest pain and ECG abnormality showing ST depression in leads V3 to V6. During the assessment in the emergency room, she developed ventricular fibrillation requiring cardioversion and 3 minutes of CPR. She was transferred to the cath lab where a critical stenosis of the circumflex was treated with percutanous coronary intervention. Her left ventricular function was normal by echocardiography and she did not require an ICD. Her prognosis is excellent.
Not all heart attacks are created equal: Type 4.
Type 4 heart attacks are usually related to a percutanous coronary intervention. In patients undergoing percutanous coronary intervention and normal troponin at baseline, an elevation of troponin > 5 x 99th percentile occurring within 48 hours of the procedure, in addition, prolonged ischemic symptoms (>20 mins of chest pain), ischemic ST changes or new Q-wave or angiographic limitation of flow, or new wall motion abnormality usually defines a Type 4 MI.
Another category of percutanous coronary intervention related MI (Type 4b MI) includes stent thrombosis. It is classified as early thrombosis (0-30 days) such as the patient below who had an occlusion of his stent just 6 hours after recanalization of his anterior myocardial infarction. The patient usually complained of recurrent chest pain with ST changes. The mechanisms involved in these circumstances usually entail a malapposition or incomplete deployment of the stent or an edge dissection. The patient was treated with additional stenting and did great.
A late stent thrombosis (31 day to 1 year) can occur when there is a change in the management of the anti-platelet therapy. The case below illustrates an example of an occlusion of the circumflex marginal coronary artery resulting from the patient discontinuing his Plavix just 2 weeks after PCI. Three months later, he presented with an acute type4 MI.
A very late stent thrombosis (> 1 year) can occur for different reasons. The most important reasons include neo atherosclerosis and malapposition of the stent that can result from the polymer.
Not all heart attacks are created equal: Type 5 MI.
Myocardial infarctions can occur after CABG particularly when reperfusion is incomplete or the bypass grafts are inadequate to provide myocardial blood flow to the ischemic areas. Other reasons include coronary dissection, global or regional ischemia due to inadequate intra operative myocardial protection. When troponin values are >10 x 99th percentile during the 1st 48 hours following CABG (from a normal baseline), or a new ECG or imaging evidence of MI or documented graft occlusion by cath, a Type 5 MI diagnosis is made.
Our patient is a 48-year-old male smoker, hypertensive, with peripheral vascular disease who had a previous bypass surgery in 2005. The patient presented to the cardiac catheterization laboratory with unstable angina. His angiogram showed a severe occlusion of the left main with diffuse disease of the RCA graft and sub occlusion of the LAD graft. The LIMA was occluded. He underwent redo CABG with right internal mammary artery (RIMA) to the LAD, vein graft to the diagonal branch and a graft to the circumflex OM using the radial artery. The vein graft to the RCA was judged to be adequate and was left alone. During surgery, the patient was found to have severe adhesions, the LAD was small, there was no vein available and the radial artery was noted to have some atherosclerosis. The patient’s course was complicated by respiratory failure, renal failure, blood loss anemia and shock liver. He was placed on full ECMO (Extracoroporeal Membrane Oxygenation), CRRT (Continuous Renal Replacement Therapy), recovered and was successfully discharged. His troponin rose to 18 and resolved to 0.7 at discharge. The patient suffered a type 5 MI and probably would have not survived if he had not been treated aggressively.
Not all heart attacks are created equal
In clinical studies, different risks have been associated with different MI subtypes. Type 2 MIs and type 4 or periprocedural MIs have been associated with increased risk of mortality, however, the hazard of death is increased four times after type 1 or spontaneous myocardial infarction. Although less frequent, patients with 4 MIs or patients with stent thrombosis, whether early or late, and patients with type 5 MIs or post CABG tend to have a worse prognosis with 10-fold increase in mortality. There is a clear adverse effect of all types of MI on mortality. Research is needed to continue to test new medical therapies. We need to emphasize the importance of secondary prevention to reduce the risk of recurrent MI and mortality.