網路內科繼續教育
有效期間:民國 92年07月01日 92年07月15日

    Case Discussion

<Brief History>

      A 71 year old woman was admitted to hospital for recurrent chest pain and increasing shortness of breath for 3 hours. She had been hospitalized about 3 months ago for unstable angina, when ECG revealed biphasic T waves in leads V1 – V4 (Figure1 ). She had a past history of type 2 diabetes controlled on drugs and hypertension. She described daily symptoms of chest pain and dyspnea with mild to moderate exertion, and had woken on two occasions at night with similar symptoms. She had no other problems, her blood sugars were satisfactory (averaging 110 to 150 mg/dl), and she reported no other features of heart failure. She had never smoked, lived by herself and was normally fully independent. Her usual medications consisted of: aspirin 100mg once per day, glipizide 5mg three times per day, and diltiazem CD 180mg once per day.

     Physical examination revealed an elderly lady in no distress at rest, with regular pulse 80 bpm, BP 140/80 with no postural drop, JVP elevated 3cm, mild ankle edema, third heart sounds with 2/6 pan-systolic murmur at the apex, and widespread crackles in the lung bases on chest auscultation. ECG (Figure2 ) at ER revealed tall ST segment elevation in leads V1 – V5, while CXR showed mild cardiomegaly with pulmonary venous congestion and small bilateral pleural effusions. Blood tests revealed mild normochromic anaemia (Hb 10.2 g/dl), elevated serum creatinine 1.6mg/dl, urea 28 mg/dl, potassium 4.9 mmol/l, and raised troponin-I to 10 U/I. Urinalysis shows 2+ proteinuria.

     Under the impression of acute anteroseptal AMI, emergent cardiac catheterization was performed and coronary angiogram showed LM short & patent, RCA patent, proximal LAD total occlusion, proximal LCX 60% stenosis; ballooning dilatation with stenting for LAD was performed with flow restoration and 0% residual stenosis . The post-procedural course was rather smooth. However, dyspnea followed by collapse was noted 5th days after infarction. BP70/40mmHg, HR124/min, grade 3/6 pan-systolic murmur at the apex, and diffuse wheezing were noted. F/U 12-lead ECG showed sinus tachycardia and Q wave in V1-4. Meanwhile, biochemistry and ABG was shown as following: BUN/Cr 36/1.8 mg/dl, AST 43 U/I, Na/K/Cl 141.6/4.53/111mM, Ca 2.06 mM, P 5.9 mg/dl, Mg 1.13 mM, CK/CK-MB/Troponin-I 70/16/14.1U/I; ABGs pH/pCO2/pO2/HCO3/BE 7.31/19.7/181.3/9.7/-15.0. Echocardiography revealed a jet from LV apical septum to RV. Intra-arterial counter-pulsation and repair for ventricular septal rupture were done soon. She was discharged 4 weeks later with improved condition.

Disscusion

     這位婦人前次住院的病情符合 Wellen's syndrome 的臨床診斷,Wellen's syndrome的定義是有典型心絞痛的病史再加上心電圖胸前導程V1-4 (尤其是V2-3)出現雙相或倒置的T 波,則可高度預期有嚴重的近端左前降枝冠狀動脈狹窄。患者因而有發生大片前壁心肌梗塞或猝死的高危險性;所以不建議做運動心電圖等壓力性檢查,而是應該及早做心導管檢查並且處理血管狹窄的問題。本病例提醒我們不應該忽略掉這些心電圖變化或是僅以保守性藥物治療的方式處理這類病人,以免延誤病情,造成更大的傷害。

參考文獻: Wellens' Syndrome, Annals of Emergency Medicine, March 1999, Vol.33, No. 3, pp347-351.

繼續教育考題
1.
(D)
What is the likely ECG diagnosis shown in figure1?
AAcute myocarditis
BAcute pulmonary embolism
CLVH
DWellen's syndrome
2.
(D)
Retrospectively, what would be your triage-management decision in her first hospitalization?
ASend the patient home and arrange follow-up with his family doctor
BAdmit the patient to a chest pain observation unit to rule-out acute coronary syndrome
CAdmit the patient to a coronary care unit to rule-out an AMI
DEnsure that the patient has an immediate coronary catheterization
3.
(C)
What is the short-term mortality rate in patients with acute chest pain syndrome who are incorrectly identified as having low risk, are dismissed from the emergency department, and subsequently suffer myocardial infarction?
AVery similar to the rate in hospitalized patients
B5%
C25%
D50%
4.
(B)
Which of the following statements about initial presentation of suspected acute coronary syndrome is true?
AOxygen should be administered throughout the hospitalization, even when the oxygen saturation rate is above 92%
BBeta-blocker therapy should be strongly considered for all patients
CCalcium channel blockers are standard therapy
DIf the initial electrocardiogram is normal, it is unlikely that the patient has an unstable coronary syndrome
5.
(C)
Mechanical complication should be considered when she suffered from dyspnea and collapse several days after AMI except
AMitral regurgitation due to papillary muscle rupture
BVentricular septal rupture
CPatent foramen ovalis
DCardiac tamponade
6.
(D)
In unstable angina, factors associated with a poorer prognosis include the following:
APrognosis is determined by the ability to control symptoms acutely, preventing progression to AMI.
BEvidence of myocardial necrosis, as determined by elevated troponin I
CDelays in angiography in patients at high risk
DAll above are included.
7.
(B)
ST-segment elevation myocardial infarction is usually caused by
ACoronary vasospasm
BThrombus superimposed on preexisting atherosclerotic plaque
CEmbolism from aortic debris
DCollagen vascular disease
8.
(D)
Which of the following medications is/are not useful in the management of acute myocardial infarction?
ANitroglycerin
BBeta-blockers
CAspirin
DAdriamycin
9.
(A)
Which of the following is not appropriate for early reperfusion therapy for ST-elevation segment myocardial infarction?
AHemodialysis
BAlteplase
CTenecteplase
DEmergency angioplasty
10.
(D)
What is true about ventricular septal rupture from myocardial infarction?
APrompt diagnosis and immediate cardiac support (IABP) is necessary to obtain a hemodynamic stabilization before surgical intervention.
BFactors most associated with this complication were advanced age, anterior infarction, female sex, et al.
CMortality at 30 days is around 75% in patients of AMI complicated with ventricular septal rupture.
DAll above are true.

答案解說

  1. (D) Wellens' syndrome is due to a near-total obstruction of the proximal anterior descending coronary artery and there is a high likelihood of an AMI in the near-future if the condition is not recognized and treated with surgery (or PCTA). A patient with Wellens' syndrome may have a normal ECG when presenting with chest pain, and then develop the characteristic ST/T wave changes in the precordial leads (usually V2 and V3, and occasionally V1 - V4) when asymptomatic. During subsequent pain- periods, the patient may also develop definite ST elevation or depression across the mid-chest leads indicative of an anterior AMI.
  2. (D) When a middle-aged or elderly patient presents to the ED with chest "tightness", all emergency physicians immediately look at the presenting ECG for any evidence of an AMI requiring thrombolytic therapy, or for any ECG evidence of an ACS requiring CCU admission and anti-cardiac ischemia therapy. This patient has a classic ECG finding that makes the clinical diagnosis and triage decision-making easy => the patient has a high-grade stenosis of the anterior descending coronary artery and she needs emergent coronary artery catheterization.
    參考資料:
    Wellens' syndrome: Tandy TK - Annals of Emergency Medicine 33 (3) 347 - 51 March 1999
  3. (C) Patients who are incorrectly identified as having low risk, are dismissed from the emergency department, and later experience an MI have a short-term mortality rate of 25%--at least twice the current mortality rate of patients with documented MI who are admitted to the hospital.
    參考資料: 
    McCarthy BD, Beshansky JR, D'Agostino RB, et al. Missed diagnoses of acute myocardial infarction in the emergency department: results from a multicenter study. Ann Emerg Med 1993;22(3):579-82
  4. (B) Oxygen should be administered when the oxygen saturation rate is below 92%. Avoid Medications that decrease survival
    i. Avoid Calcium Channel Blockers (esp. Dihydropyridines)
    ii. Avoid Antiarrhythmics
    Beta blockers is indicated in all patients without contraindications. Even though the initial electrocardiogram is normal, it is likely that the patient has an unstable coronary syndrome.
    參考資料: 
    Braunwald E, Antman EM, Beasley JW, et al: ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2000 Sep; 36(3): 970-1062
  5. (C) Cause of hypotension of acute MI:
    I. Arrhytmias
    1. VF / VT (Primary VF; Secondary VF; Late VF)
    2. Asystole
    3. heart blocks (usually temporary if with inferoposterior AMI and permanent if with anterior!)
    4. atrial fibrillation (increases mortality!)
    5. premature beats (most common, usually not requires Rx!)

    II. Pump failure
    1. Acute CHF, pulmonary oedema
    2. cardiogenic shock
    3. acute right heart failure

    III. Wall rupture, tamponade, ventricular septal rupture
    IV. Acute mitral regurgitation (papillary muscle or tendon rupture)
    V. Vagal stimulation: “hypotonia-bradycardia syndrome”(inferoposterior AMI)
  6. (D) In unstable angina, factors associated with a poorer prognosis include the following:
    1. The ability to control symptoms acutely, preventing progression to AMI.
    2. Evidence of myocardial necrosis, as determined by elevated troponin I.
    3. Early intervention in patients at high risk
  7. (B) Numerous studies have now linked acute coronary syndrome with rupture of the thin fibrous cap of the atherosclerotic plaque followed by release of highly thrombogenic material into the vascular lumen. Careful studies have found a 79 to 98 percent correlation between these findings. Therefore, ST-segment elevation myocardial infarction is usually caused by thrombus superimposed on preexisting atherosclerotic plaque
  8. (D)
  9. (A)
  10. (D) In GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial, 84 of the 41 021 patients (0.2%) developed VSD, a smaller percentage than reported: in the prethrombolytic era. The mean interval between myocardial infarction (MI) and VSD was: 3.6+/-4.1 days. The median time from symptom onset to VSD diagnosis was 1 day. Enrollment factors most associated with this complication were advanced age, anterior infarction, female sex, and no previous smoking. The infarct artery was more often the left anterior descending and more likely to be totally occluded in patients who developed VSD. Mortality at 30 days was higher in patients with VSD than in those without this complication (73.8%: versus 6.8%, P<0.001). Patients with VSD selected for surgical repair (n=34) had better outcomes than patients: treated medically (n=35; 30-day mortality, 47% versus 94%).
    參考資料: 
    Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute: myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial: Investigators. Circulation. 101(1):27-32, 2000 Jan 4-11.

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