Effective superpotential and vacuum structure

Table 17.4: Atypical features of aortic dissection

•  Occlusion of neck vessels 

•  Aortic valve regurgitation 

•  Left ventricular dysfunction 

•  Myocardial infarction 

•  Pericardial effusion 

Table 17.2: Typical features of aortic dissection

•  Dilatation of the proximal aortic root > 42 mm

The complications of aortic dissection are related to the involvement of the aortic valve, pericardial sac and the arteries emerging from the aorta. Proximal involvement of the aortic valve can cause acute aortic regurgitation and heart failure. Hemorrhagic pericardial effusion can cause cardiac tamponade. Involve-ment of the coronary artery ostium can actually lead to myocardial infarction (Table 17.4). Involvement of the subclavian arteries can cause upper limb ischemia and discrepancy between the radial pulse volume on both sides. Involvement of carotid arteries can cause cerebral ischemia as in our case, who had weakness of the left hand and a right-sided carotid bruit. In distal aortic dissection, there may be mesenteric, renal, spinal cord or lower limb ischemia (Fig. 17.2).

There are various classifications of aortic dissection. The simplest classification is of the Stanford group, which categorizes dissection as Type A (proximal), where the ascending aorta is involved and Type B (distal), where the ascending aorta is spared. This classification has prognostic as well as therapeutic implications.

DeBakey Type I dissection extends from the ascending to descending aorta while Type II is confined to the ascending aorta. Type III is confined to the descending aorta and akin to Stanford Type B (Table 17.3).

Table 17.3: Classification of aortic dissection according to location DeBakey type Stanford group Location of dissection Incidence I

II 

A Ascending to descending aorta 10%

Confined to ascending aorta  70%

III  B Confined to descending aorta  20%

}

80 Section 5 Aortic Diseases

MANAGEMENT ISSUES

The management of aortic dissection depends upon its location and extent, the presence or absence of complications and the hemodynamics of the patient.

In distal (Type B) dissection, it generally suffices to control the blood pressure adequately. Agents with negative ionotropic effect such as a beta-blocker or verapamil are preferable as they reduce the shearing force on the aorta and the progression of dissection. A vasodilator such as sodium nitroprusside or an ACE-inhibitor may be added if the blood pressure remains significantly elevated. In the presence of abdominal, spinal or lower limb severe ischemia, an endovascular stent graft may be deployed to cover the dissection.

In proximal (Type A) dissection, surgical intervention is preferable unless the hemodynamics are compromised, in which case a conservative approach is adopted. The affected segment of the ascending aorta is resected and replaced with a prosthetic graft. The aortic valve and coronary ostia may need to be reconstructed. In extensive aortic dissection (DeBakey Type I), a combined approach that includes proximal resection with graft and distal endovascular stenting may be used.

RECENT ADVANCES

Newer imaging techniques such as computed tomographic (CT) angiography and magnetic resonance imaging (MRI) have obviated the need for aortography, in the evaluation of aortic dissection. The sensitivity and specificity of these tests, for a confirmatory diagnosis of aortic dissection, are in excess of 95%. The technique of percutaneous endovascular stenting to manage DeBakey Type I and III dissection, has also undergone considerable refinement.

Figure 17.2: Complications of aortic dissection

C A S E

18 Coarctation

of Aorta

CASE PRESENTATION

A young man 27 years of age, presented to the out-patient clinic with general fatigue and difficulty in climbing even two flights of stairs. He was diagnosed to have systemic hypertension five years back and had been on antihypertensive drugs ever since. Besides his fatigue, he also complained of episodic headache with dizziness.

These episodes were often related to undue physical exercise, emotional upset or to missing of his medication. There was no history of cyanotic spells or fleeting joint pains during childhood. He denied abusing tobacco, alcohol or illicit drugs.

On examination, there were no facial features of an endocrine disorder such as thyrotoxicosis, acromegaly or Cushing’s syndrome, but his lower limbs were unusually thin. The radial pulse was 84 beats/min. and bounding in nature. The BP in his right arm was 170/100 mm Hg. Pulse amplitude over the femoral arteries was reduced in volume and delayed compared to the brachial pulsation. Also, there were visible pulsations in the suprasternal notch. The cardiac apex beat was heaving in nature and slightly displaced towards the left axilla. On auscultation, S₁ was normal, A₂ was loud and a presystolic S₄ was audible. An ejection systolic murmur was heard at the upper left parasternal area. Incidentally, the same murmur was also audible over the interscapular region. Soft continuous murmurs were also heard over the scapulae.

On abdominal auscultation, there was no bruit heard over the renal arteries.

CLINICAL DISCUSSION

When confronted with a young patient with moderate to severe systemic hypertension, the clinician should be alert to the possibility of secondary hypertension. Incidentally, secondary hypertension constitutes less than 5% of all hypertensive patients, while most have primary or essential hypertension.

Usual causes of secondary hypertension are:

• Endocrine disorders

• Renovascular disease

• Coarctation of aorta.

In this patient, ECG showed tall R waves in leads V₅ and V₆ with deep S waves in leads V₁ and V₂, indicating the presence of left ventricular hypertrophy (Fig. 18.1). X-ray showed mild cardiomegaly with a rounded contour of the left heart border. There was “notching” of the undersurface of the 4^th to 8^th ribs and

82 Section 5 Aortic Diseases

a “figure-of-3” appearance of the aortic arch. ECHO revealed concentric left ventricular hypertrophy with normal ejection fraction. Aortic valve was bicuspid with thickened leaflets and an insignificant gradient across the valve. The mitral valve was normal and there was no ventricular septal defect. Doppler signal from the suprasternal notch showed a pulsatile aortic arch with a distal aortic gradient that tapered into diastole. A mosaic jet was seen in the descending aorta, directed away from the transducer (Fig. 18.2).

Figure 18.1: ECG showing tall R waves in V₅,V₆ with deep S waves in V₁,V₂

Figure 18.2: ECHO showing a mosaic jet in the descending aorta

Coarctation of aorta is the most likely cause of hypertension in this case.

There was clinical, radiological and cardiographic evidence of left ventricular hypertrophy. There were brachio-femoral delay, suprasternal pulsations, a parasternal and interscapular systolic murmur (coarctation itself) and continuous intercostal murmurs (collateral vessels). All these auscultatory findings are pathognomic of aortic coarctation. The murmur of coarctation itself may be continuous if the narrowing is severe, while presence of an ejection click indicates an associated bicuspid aortic valve. On X-ray chest, notching of the lower border of ribs indicates arterial collateralization, to by-pass the aortic obstruction. The

“figure-of-3” appearance is produced by indentation of the aorta at the site of coarctation, with dilatation on either side of the narrowing. The suprasternal high velocity Doppler signal is characteristic of aortic coarctation.

Coarctation of the aorta is a localized narrowing of the aortic arch (Fig. 18.3), due to a fibrous ring encircling the wall or a shelf projecting into the lumen. The narrowing is in the region of the ligamentum arteriosum (juxta-ductal) and may be pre-ductal or post-ductal. The aorta distal to the narrowing is often dilated and aneurysmal. Coarctation may present in the neonatal period (infantile type)

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