Aortic regurgitation resulting from blunt chest trauma has been reported only 95 times, to our knowledge. The noncoronary and right coronary cusps are the cardiac structures most often injured. Although the aortic leaflets can appear to be undamaged after nonpenetrating trauma, they can have pathologic abnormalities and insufficient function. Some cases of posttraumatic aortic regurgitation progress slowly. Aortic valve replacement is the optimal treatment. We present the case of a then-62-year-old man who has lived more than 5 years after blunt-trauma aortic regurgitation. His is the only case of long-term survival on medical therapy alone among the 96 cases summarized in this report.
Traumatic aortic regurgitation (AR), an infrequently reported sequela of blunt chest trauma, is characterized by a history of such trauma, a normal-appearing heart during post-trauma examination, subsequent aortic insufficiency of sudden onset, and the exclusion of other causes of aortic incompetence.1 Traumatic AR has typically been diagnosed early after chest trauma; however, 18% of the reported cases were diagnosed after one year because of slowly progressive degenerative patterns. The noncoronary cusp (NCC) and right coronary cusp (RCC) were injured in 73% of reported instances. Aortic valve replacement (AVR) has led to a good prognosis (mortality rate, 1%). Aortic valvuloplasty has yielded poorer results, and previous outcomes from medical therapy alone were uniformly fatal. We report the case of our medically treated AR patient, and we summarize the other published reports of blunt-trauma AR.
Case Report
In July 2011, a 62-year-old man, who had never had heart murmurs during annual medical checkups, was driving his car on the highway and sustained a chest bruise from a stone that crashed through his windshield. At a subsequent clinical visit, no abnormalities were detected. However, 6 months later, he had a grade 3/6 diastolic murmur, audible at the left sternal border. At our hospital, he reported no chest discomfort. Transesophageal echocardiograms revealed moderate AR caused by prolapse of the RCC (Fig. 1). The diagnosis was traumatic AR, on the basis of the following criteria1: the patient's history of trauma, his normal-appearing heart upon recent physical examination, the sudden onset of aortic insufficiency, and our exclusion of other causes of aortic incompetence. Transthoracic echocardiograms showed that the patient's left ventricular systolic diameter was 37 mm; diastolic diameter, 56 mm; and ejection fraction, 0.63. Surgical treatment did not seem to be indicated, and we prescribed medical therapy (olmesartan 20 mg/d and enalapril 5 mg/d). During the last 2 years, the patient's clinical and echocardiographic status has gradually deteriorated (Table I). Although surgical treatment is indicated at the time of this report, he declines to undergo an operation.
Discussion
Nonpenetrating cardiac traumas can result in rapid death from cardiac tamponade. From 1955 through 2015, 95 cases of AR after blunt trauma were described (Table II). Counting our patient, traumatic AR has been diagnosed in 85 men and 11 women (age range, 5–83 yr; median, 44 yr). The causes were automobile accidents in 49 instances, motorcycle accidents in 18, falls in 12, falling objects in 6, sports injuries in 4, and other causes in 7. The time from the index incident to the diagnosis of traumatic AR ranged from immediately to 10 years or longer: 34 cases were diagnosed within 3 days,2–34 20 within 1 month,1,35–54 12 within 3 months,45,55–64 5 within 6 months,165–68 4 within 1 year,32,69–71 2 within 2 years,72,73 2 within 3 years,74,75 5 in over 5 years,65,76–78 and 12 after an unspecified duration.79–88 Early diagnoses (within 3 d) were 35% of the total; in the other patients, AR apparently progressed slowly.
Table III shows which cardiac structures were injured. Chief among these were the NCC and the RCC (in 71 of 96 instances). The left coronary cusp—injured far less often—might be protected by its coronary arteries, which perfuse a large area and might serve as buffers against high hydrostatic pressures.
We summarize the treatment outcomes of the 96 patients, in Table IV. Of 70 patients who underwent AVR, 62 had a good outcome, and only 1 patient died (mortality rate, 1%). The other 7 outcomes were unspecified. Aortic valvuloplasty yielded good outcomes in 13 of 20 patients, new-onset AR murmurs in 4, and 2 deaths. In stark contrast, of the 6 patients who were prescribed medical therapy alone, only our patient survived—now longer than 5 years.
On macroscopic examination, the aortic leaflets can appear to be undamaged when instead they are pathologically abnormal,18 and this can cause valvular insufficiency. German and colleagues13 reported up to an 80% recurrence of aortic insufficiency after valvuloplasty and recommended AVR for treating traumatic AR. Some authors31,32,78 have reported good results after valvuloplasty, but the long-term outcomes in those cases are unknown.
Our patient's experience and our review of the earlier cases indicate that AR from blunt trauma can gradually worsen. Therefore, patients thus affected should be carefully monitored, and AVR instead of repair should be the treatment of choice.
Contributor Notes
From: Department of Cardiology (Drs. Mahara and Tsugu), Sakakibara Heart Institute, Fuchu 183-0003; Departments of Cardiology (Drs. Fukuda and Tsugu) and Laboratory Medicine (Dr. Murata), School of Medicine, Keio University, Tokyo 160-8582; and Department of Cardiology (Dr. Iwanaga), Saitama International Medical Center, Saitama 350-1298; Japan