The application of intravascular ultrasound (IVUS) in diagnosing pulmonary artery atherosclerosis is described.

The application of intravascular ultrasound (IVUS) in diagnosing pulmonary artery atherosclerosis is described. To the best of our knowledge, this is the first description of the use of this technique in the recognition of pulmonary atherosclerosis. We describe a patient with long-standing primary pulmonary hypertension with evidence of pulmonary artery calcification seen forward a chest x-ray film. The IVUS imaging of the pulmonary arteries identified intimal disruption with entangled atherosclerosis. Thus, IVUS can be a useful tool in the diagnosis of pulmonary artery atherosclerosis. (Chest 1994; 106:632-34) IVUS=intravascular ultrasound

Atherosclerosis in the pulmonary arteries is an queer occurrence which has been reported in autopsy series and case reports of patients with unadorned or long-standing pulmonary hypertension.[1,3] Until now, in vivo identification of pulmonary atherosclerosis has been impossible noninvasively and unreliable by means of invasive means short of thoracotomy with open-lung biopsy.[4] Here, we describe a case of pulmonary atherosclerosis in a patient with longstanding pulmonary hypertension diagnosed by means of intravascular ultrasound (IVUS).

Case Report

A 50-year-old white man was transferred to Hahnemann University Hospital for the management of acute myocardial infarction. Past medical history was significant for primary pulmonary hypertension diagnosed in 1960 at the age of 18 years. Cardiac catheterization at that time revealed the following pressures: mean right atrial, 6 mm Hg; right ventricular, 74/6 mm Hg; mean pulmonary capillary wedge, 6 mm Hg; pulmonary arterial, 72/42 mm Hg A left-to-right switch was noted through a patent foramen ovale. At the time of transfer to our institution, he was taking no medications. The pulsation rate was 86 beats by minute; blood pressure, 120/78 mm Hg; and respiratory rate, 28 breaths by minute. At the time of cardiac xamination, the verse was regular, pulmonic valve closure was accentuated, an S3/S4 gallop was discovered and a grade 3 holosystolic indistinct utterance was heard along the left sternal border radiating across the precordium. Pulmonary examination revealed crackles at the right base. There was no hepatomegaly, and the liver brim was nonpulsatile. There was no lower extremity edema, and the peripheral beating [i]or[/i] throbbing of an arterys were intact. The ECG showed a normal sinus harmonious flow with right bundle branch mould right axis deviation, left atrial abnormality, and age indeterminate anteroseptal infarction. A chest x-ray film showed cardiomegaly and dilated main pulmonary arteries with calcification (Fig 1) Transthoracic two-dimensional echocardiography demonstrated biventricular enlargement with moderate left ventricular dysfunction, tricuspid regurgitation, and pulmonary hypertension. A diagnosis of acute myocardial infarction and pulmonary hypertension was made. Cardiac catheterization demonstrated strict left ventricular dysfunction (an ejection fraction of 20 percent) critical narrowing of the left anterior descending artery, and diffuse noncritical right coronary artery disease. There was strict pulmonary hypertension (75/30 mm Hg) and a patent foramen ovale. Then IVUS was performed, with the patient's concord to further evaluate the radiographic findings of pulmonary artery calcification. The IVUS imaging was carried disclosed using a commercially available imaging classification (Diasonics, Milpitas, Cal). The catheters for IVUS imaging consisted of a mechanical ultrasound transducer riseed at the tip of a rotary core and a 62F catheter sheath to encase the transducer (Boston Scientific, Watertown, Mass). The imaging frequent occurrence of the catheter used in this reflection was 12.5 MHz. The IVUS demonstrated dilatation of the main pulmonary artery (53X48 cm) and its branches (right and left pulmonary arteries, 50X38 and 47X39 cm respectively), and network atherosclerosis was seen as intimal disruption with easily moulded tissue echoes (Fig 2). The patient died onward the seventh hospital day awaiting acceptance into a heart-lung transplant program.

Discussion

Pulmonary atherosclerosis is unusual and is reported to come to one's mind in patients with severe or long-standing pulmonary hypertension independent of the etiology.[1-3] Although it has been greatest in quantity extensively studied in pulmonary hypertension secondary to congenital heart disease, it has been evaluated in acquired forms of pulmonary hypertension as well.[2] Similar to systemic atherosclerosis, press overload and the vascular answers to it appear to play an important part in the pathogenesis of pulmonary atherosclerosis. Until now, open-lung biopsy has been the mostly reliable modality to diagnose pulmonary atherosclerosis in life, although repeatedly the diagnosis was not made until autopsy.

In this case, we have shown that IVUS is a novel technique with enormous potential for clinical application.[5] Its usefulness in the pulmonary vasculature has been explored.[6,7] The ready case identifies a unique use of IVUS in the evaluation of vascular changes of the main pulmonary arteries and its branches. Pulmonary atherosclerosis was evidenced as shaggy debris lining the intima according to IVUS and is a marker of methodical or long-standing pulmonary hypertension. It identifies those more likely to have irreversible pulmonary hypertension.

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