When the pressure within the aortic wall exceeds a critical limit rupture occurs, either into the pericardium with cardiac tamponade or into the pleural space or mediastinum 9. Emergency aortic repair together with intra-operative pericardial drainage is the recommended treatment approach. However, there is controversy about performing pericardiocentesis in patients who are hemodynamically unstable and while awaiting surgical repair 10 , Pericardiocentesis is the treatment of choice for cardiac tamponade caused by various diseases, but in case of hemopericardium complicating AD drainage can aggravate the leak or rupture However, according to the recent published guidelines for the diagnosis and management of patients with thoracic aortic disease, preoperative pericardiocentesis can be lifesaving when managing patients with cardiac tamponade with pulseless electrical activity or refractory hypotension complicating acute type A aortic dissection, especially when cardiac surgery is not immediately available 9 , Two pathophysiological mechanisms have been proposed to explain a branch vessel compromise associated with AD; static, where the expanding hematoma cause narrowing of the affected vessel, and dynamic; where the dissection flap can partially occlude the ostium of an artery, affecting the blood flow inside the vessel, which may lead to coronary thrombosis and consequent myocardial infarction MI if coronary arteries are involved 13 - In addition, the dissection can extend directly into the coronary arteries from the aorta, and usually the right coronary artery is more often affected than the left Usually it is difficult to differentiate between myocardial ischemia and AD in patients presenting with sudden onset chest pain, also EKG may show ST segment elevation and signs of acute transmural MI when the coronary arteries are involved by the mechanisms described above.
Bedside echocardiography is a quick noninvasive method to detect wall motion that can be utilized in cases of chest pain when aortic dissection is a concern.
Patients can be divided to 3 groups: low, intermediate, and high risk based on historical and examination. The ADD risk score has a In cases of AD associated with MI, and coronary artery dissection or compression by the expanding hematoma; treatment with coronary artery stenting or positioning of a coronary perfusion catheter will help to maintain an adequate coronary perfusion, and reduce myocardial ischemia until surgical repair is done 20 - This case presentation of aortic dissection mimicking inferior MI and complicated with pericardial tamponade represents a rare and fatal combination of sequelae.
Medical therapy is minimal initially since immediate surgical intervention is required. This is aimed at reducing blood pressure and the shear force on the aorta. Calcium channel blockers and nitrates can also be helpful.
Caution is advised when lowering blood pressure during acute ascending aortic dissection since shock can occur from the many possible complications.
Aortic regurgitation : Acute aortic regurgitation can result from dilation of the aortic root. This may cause acute left heart failure with hypotension and pulmonary edema. Inferior myocardial infarction : When the ascending aortic dissection involves the ostium of the right coronary artery, an inferior myocardial infarction can occur. Treatment is emergent coronary bypass surgery. Cardiac tamponade : An acute pericardial effusion can occur causing cardiac tamponade if the proximal portion of the ascending aortic dissection ruptures into the pericardium.
In this situation physical exam findings include:. A total of one liter of hemorrhagic fluid was drained. Pericardial tissue biopsy showed acute and chronic inflammatory cells with thickened pericardium, and no malignant cells were detected Figure 3. Tuberculosis quantiferon assay, acid-fast bacilli staining, and fungal and bacterial cultures of the pericardial tissue were negative. The source of pericardial effusion remained elusive. Given the hemorrhagic nature of the pericardial effusion in the absence of recent use of anticoagulation and the negative workup for infectious or autoimmune etiology, a CT scan of the chest with contrast was obtained to evaluate for possible malignancy.
CT showed an ascending aortic aneurysm measuring up to 7. The patient underwent successful open surgical repair of his chronic Stanford type A aortic dissection with an uneventful postoperative course. Acute Stanford type A aortic dissection AD is a life-threatening condition that serves as an impetus to immediate surgical repair aiming to prevent dissection-associated complications such as acute aortic regurgitation, aortic rupture, myocardial or cerebral ischemia, and pericardial tamponade [ 1 ].
However, newly diagnosed chronic type A CTAD dissections of a native aorta represent a different subpopulation of patients with atypical or absent symptoms at the time of dissection onset precluding the early diagnosis [ 2 — 4 ]. Patients with de novo chronic AD are usually asymptomatic at the time of diagnosis like our patient [ 2 ]. Thus, newly diagnosed CTAD is usually discovered incidentally upon chest imaging as a prominent aortic knob or mediastinal widening [ 2 ].
Therefore, the accurate timing of dissection is often unfeasible [ 2 ]. Careful history is needed to identify previous acute chest pain events heralding dissection onset. Furthermore, the patient may endorse symptoms related to the enlarging dissection e.
Features like thick, immobile intimal flap, aneurysmal dilatation of the thoracic aorta as in our patient , or the presence of thrombus in the false lumen are suggestive of dissection chronicity [ 2 ]. Signs of contained rupture such as pleural effusion or mediastinal hematoma can also be seen in symptomatic patients [ 2 ]. Pericardial effusion is a common complication of acute type A AD and usually occurs through two separate mechanisms [ 5 ].
The first mechanism is the transudation of fluid across the thin wall of the false lumen into the pericardial cavity which is the most common mechanisms [ 5 ].
However, the dissected aorta can rupture directly into the pericardial space with subsequent tamponade [ 5 ]. In our case, CTAD was asymptomatic and initially was not clinically suspected; thus, pericardial puncture was carried out for the evaluation of the pericardial effusion. Our patient was hemodynamically stable with no contraindications for contrast administration.
Given the negative pericardial fluid analysis, the 20 pack-years of smoking, and the thyroid cancer history, hemorrhagic pericardial effusion secondary to metastatic cancer was suspected. Thus, a CT scan of the chest with contrast was obtained and aortic dissection was incidentally discovered.
The first clue for CTAD diagnosis was the detection of high-density pericardial effusion note on abdominal CT scan before elective cholecystectomy. Given the lake of symptoms, transudation of fluid across the wall of the false lumen into the pericardial cavity is the most plausible mechanisms. We combined pre-, peri- and postoperative mortality until hospital discharge of unselected ED patients, who were included in the study on an intention to treat basis.
In the present analysis, signs of preoperative severe cardiac tamponade without palpable pulses were associated with poor outcome, particularly preoperative death. This finding is supported by several former observations with regard to in-hospital death [4 , 8 , 10]. All preoperative deaths in our patients were due to severe cardiac tamponade. We found impending cardiac tamponade in patients with palpable pulses not to be associated with adverse outcome.
The frequency of severe cardiac tamponade was rather low in the present patient series, particularly if compared to the frequency of hemodynamic shock. This may be explained by the relatively frequent occurrence of other severe complications of type A aortic dissection in these patients such as hemothorax due to free rupture. Furthermore, this discrepancy may be due to a partial overlap of the definitions of hemodynamic shock systolic blood pressure below 90 mmHg and impending cardiac tamponade tamponade with palpable pulses.
The fact that severe cardiac tamponade has an adverse effect on preoperative outcome in patients with acute type A aortic dissection is a well-known notion. Similarly, we found that the vast majority of these patients died preoperatively. However, remarkably impending cardiac tamponade with palpable pulses was, per se, not associated with poor pre-, peri- or postoperative outcome in the present patient series. But if systolic blood pressure values deteriorate below 90 mmHg, these patients are at higher risk for poor outcome.
Our findings suggest that patients with type A aortic dissection and severe cardiac tamponade are at high risk for preoperative death, even when aggressive treatment with pericardiocentesis or surgical drainage is initiated.
Therefore, timely diagnosis and immediate surgery are mandatory. Immediate surgery may avert progression to severe cardiac tamponade and hemodynamic deterioration.
Similarly others found that early diagnosis and early treatment of acute aortic dissection before development of cardiac tamponade improved the operative salvage rate [1 , 7 , 8 , 20]. In conclusion, patients with acute type A aortic dissection and signs of preoperative severe cardiac tamponade without palpable pulses had a fold increased risk for poor outcome, particularly preoperative death.
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Acute type A aortic dissection: the prognostic impact of preoperative cardiac tamponade.
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