가슴이 아파요? Untable angina, NSTEMI

음.. 일하다 보면 가슴 아프다고 하면.. 참 그랬습니다.

무얼 물어봐야 하는지. 그리고 그눔의  'Typical chest pain'이 뭔지도 몰랐기 때문이지요. 답답한 일입니다.

이렇게 1년을 버텼던 것이 이제야 해리슨 책을 보고 아..~ 그려.. 그때 그 환자가 이렇게 아팠다 표현했을때 

이것이 그냥 표현이 아니었구나.. 교과서 내용이 었음을 깨닫는 순간입니다. 

(이번 내용의 참조는 해리슨 18판 244장 UA & NSTEMI 입니다.)

Patients with ischemic heart disease fall into two large groups: patients with chronic coronary artery disease (CAD) who most commonly present with stable angina(Chap. 243) and patients with acute coronary syndromes (ACSs). The latter group, in turn, is composed of patients with acute myocardial infarction (MI) with ST-segment elevation on their presenting electrocardiogram (ECG) (STEMI; Chap. 245) and those with unstable angina (UA) and non-ST-segment elevation MI (UA/NSTEMI; Fig. 245-1). Every year in the United States, approximately 1 million patients are admitted to hospitals with UA/NSTEMI as compared with 300,000 patients with acute STEMI. The relative incidence of UA/NSTEMI compared to STEMI appears to be increasing. More than one-third of patients with UA/NSTEMI are women, while less than one-fourth of patients with STEMI are women.

그렇군요. 

IHD(ischemic heart disease) 는 크게 Stable angina 와 ACS(Acute coronary syndrome)으로 나뉩니다. 

그리고 ACS는 STEMI, NSTEMI, Unstable angina로 나뉩니다. 

여기에서는 UA, NSTEMI의 정의에 대해 알아 봅니다. 

The diagnosis of UA is based largely on the clinical presentation. Stable anginapectoris is characterized by chest or arm discomfort that may not be described as pain but is reproducibly associated with physical exertion or stress and is relieved within 5–10 minutes by rest and/or sublingual nitroglycerin (Chaps. 12 and 343). UA is defined as angina pectoris or equivalent ischemic discomfort with at least one of three features: (1) it occurs at rest (or with minimal exertion), usually lasting >10 minutes; (2) it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or (3) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously). The diagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflected in elevated cardiac biomarkers.

UA는 증상적 진단이군요. 

Stable angina pectoris: physical exertion, stress에 의해 유발되는 chest discomfort, arm discomfort 이며 rest 또는 NTG에 의해 5분이내에 subside 되는 증상을 특징으로 합니다. 

Unstable angina: 다음 3가지중 1가지 이상의 특징을 가지는 angina pectoris 지요

(1) 휴식시(또는 약간의 활동)시 10분 이상 지속되거나

(2) 4~6 주 이내에 새로 발생하는 심한 증상 이거나

(3) Crescendo pattern (점차 빈도와 세기, 지속시간이 이전보다 증가하는 양상의) 인 경우 이며

NSTEMI: UA 임상양상 + Myocardial necrosis (예를 들어 enzyme elevation) 동반된 경우

UA/NSTEMI is most commonly caused by a reduction in oxygen supply and/or by an increase in myocardial oxygen demand superimposed on a lesion that causes coronary arterial obstruction, usually an atherothrombotic coronary plaque. Four pathophysiologic processes that may contribute to the development of UA/NSTEMI have been identified: (1) plaque rupture or erosion with a superimposed nonocclusive thrombus, believed to be the most common cause; in such patients, NSTEMI may occur with downstream embolization of platelet aggregates and/or atherosclerotic debris; (2) dynamic obstruction [e.g., coronary spasm, as in Prinzmetal's variant angina (PVA) (p. 2020)]; (3) progressive mechanical obstruction [e.g., rapidly advancing coronary atherosclerosis or restenosis following percutaneous coronary intervention (PCI)]; and (4) UA secondary to increased myocardial oxygen demand and/or decreased supply (e.g., tachycardia, anemia). More than one of these processes may be involved.

Among patients with UA/NSTEMI studied at angiography, approximately 5% have stenosis of the left main coronary artery, 15% have three-vessel CAD, 30% have two-vessel disease, 40% have single-vessel disease, and 10% have no apparent critical epicardial coronary artery stenosis; some of the latter may have obstruction of the coronary microcirculation. The "culprit lesion" may show an eccentric stenosis with scalloped or overhanging edges and a narrow neck on angiography. Angioscopy has been reported to show "white" (platelet-rich) thrombi, as opposed to "red" (fibrin- and cell-rich) thrombi; the latter are more often seen in patients with acute STEMI. Patients with UA/NSTEMI frequently have multiple plaques at risk of disruption (vulnerable plaques). 

UA/NSTEMI 모두 심근의 산소 공급이 저하될때 발생하는 것 이겠지요

ㅡ..ㅡ 당연하겠지요.

(1) thrombus plaque rupture 되면 당연히 생기겠지요.

(2) Dynamic obstruction 생기면 당연히 생기겠지요?, coronary spasm, Prinzmental's varient angina

(3) Progressive mechanical obstruction (Atheroscerosis 또는 Stent restenosis)

(4) Tachycardia, anemia 등의 산소 허혈 환경에서 충분히 가능한 일이겠지요.

실제 UA/NSTEMI 는 5% Lt main coronary artery stenosis 15% CAOD-3VD, 30% CAOD -2VD, 40% CAOD-1VD, 10% minimal CAOD 가능성이 있습니다. 헐. 쫌 무섭네요.

임상 양상을 봅니다. 이것은 정말 중요한 것인데요.

임상의사이기 때문이겠지요.

The clinical hallmark of UA/NSTEMI is chest pain, typically located in the substernal region or sometimes in the epigastrium, that radiates to the neck, left shoulder, and/or the left arm (Chap. 12). This discomfort is usually severe enough to be described as frank pain. Anginal "equivalents" such as dyspnea and epigastric discomfort may also occur, and these appear to be more frequent in women. The physical examination resembles that in patients with stable angina (Chap. 243) and may be unremarkable. If the patient has a large area of myocardial ischemia or a large NSTEMI, the physical findings can include diaphoresis; pale, cool skin; sinus tachycardia; a third and/or fourth heart sound; basilar rales; and, sometimes, hypotension, resembling the findings of large STEMI.

Substernal, epigastric pain (가끔 frank pain) 이면서 neck, Lt shoulder, Lt arm(ulnar side) 로 방사되는 통증(불편감)입니다.

NSTEMI 범위가 큰경우에는 diaphoresis(식은땀), 창백해지거나, 차가운 피부, 때로는 STEMI 처럼 저혈압이 생기기도 합니다. 

EKG 변화는 

In UA, ST-segment depression, transient ST-segment elevation, and/or T-wave inversion occur in 30 to 50% of patients. In patients with the clinical features of UA, the presence of new ST-segment deviation, even of only 0.05 mV, is an important predictor of adverse outcome. T-wave changes are sensitive for ischemia but less specific, unless they are new, deep T-wave inversions (0.3 mV).

 UA에서는 ST depression, transient ST elevation, T wave inversion 이 30~50%에서 발생합니다. ST deviation이 05mV만 있어도 예후에는 좋지 않답니다. 

Cardiac enzyme은

Patients with UA/NSTEMI who have elevated biomarkers of necrosis, such as CK-MBand troponin (a much more specific and sensitive marker of myocardial necrosis), are at increased risk for death or recurrent MI. Elevated levels of these markers distinguish patients with NSTEMI from those with UA. There is a direct relationship between the degree of troponin elevation and mortality. However, in patientswithout a clear clinical history of myocardial ischemia, minor troponin elevations have been reported and can be caused by congestive heart failure (CHF), myocarditis, or pulmonary embolism, or they may be false-positive readings. Thus, in patients with an unclear history, small troponin elevations may not be diagnostic of an ACS.

Small troponin elevation은 다른 CHF, myocarditis, pulmonary embolism 에서도 가능하므로  꼭 참고해야 합니다.

DIAGNOSTIC PATHWAYS

Risk Stratification and Prognosis

이 경우에는 CAG indication 입니다. 바로 응급협진의 indication 이 될수도 있겠군요.