Inhibition of arterial thrombogenesis by quinapril but not losartan.

The cardioprotective effect of angiotensin converting enzyme (ACE) inhibitors and angiotensin type I (AT1) receptor blockers may relate to their antithrombotic effect. We determined the differential effects of the ACE inhibitor quinapril and the AT1 receptor blocker losartan on arterial thrombus formation in the rat. Sprague-Dawley rats were fed regular chow or chow mixed with low-dose quinapril (0. 6 mg/kg/day), high-dose quinapril (1.2 mg/kg/day), or losartan (10 mg/kg/day) for 15 days. Abdominal aorta was exposed and wrapped with Whatman paper impregnated with 29% FeCl(3) (ferric chloride). Time to occlusive thrombus formation and weight of the thrombus were recorded. Aortic superoxide anion generation, platelet aggregation, plasma angiotensin II levels, and morphology of the thrombus were also examined. Both losartan and quinapril caused similar reductions in arterial pressure. Losartan did not affect the time to thrombus formation, whereas quinapril (both low and high doses) delayed the time to thrombus formation (P<.01 vs control). Weight of the thrombus was similar in all groups of rats. Platelet aggregation was inhibited by approximately 50 in both quinapril- and losartan-treated rats. The high-dose quinapril-treated rats showed markedly reduced vascular superoxide anion generation compared with the control rats (P<.05). Plasma angiotensin II levels were unaffected by quinapril treatment but were elevated 7-fold in losartan-treated rats (P <.001 vs. control rats). The thrombi in the control rats consisted of platelet aggregates, fibrin, and red blood cells. The intravascular platelet aggregates were much smaller in the quinapril-treated rats (P<.05 vs. control), but were similar in control and losartan-treated rats. In conclusion, quinapril but not losartan prolongs time to arterial thrombus formation and results in smaller platelet aggregates in the thrombus. Both quinapril and losartan decrease platelet aggregation, but only quinapril decreases superoxide anion generation. This effect on superoxide anion generation as well as mechanisms other than AT1 receptor blockade may underlie the salutary effect of quinapril on arterial thrombogenesis.

Unusual presentation of hemoptysis in a 78-year-old with previous Nissen fundoplication.

A 78-year-old individual, who had a previous transthoracic Nissen fundoplication 20 years earlier, presented to our institution with hemoptysis. Initial workup included chest roentgenogram, upper gastrointestinal series, and upper endoscopy, all of which were nondiagnostic. A repeat upper endoscopy diagnosed a gastrobronchial fistula by revealing a large gastric ulcer that penetrated into the lung parenchyma. The patient underwent surgery for takedown of the fistula. One of the most common symptoms associated with gastrobronchial fistula is hemoptysis, although insidious cough, recurrent pneumonia, or gastrointestinal bleeding are also observed. The most useful diagnostic study is an upper gastrointestinal series, which must be read with a high index of suspicion. Gastrobronchial fistula is most commonly a long-term complication from hiatal hernia repair. The most frequently used procedure for repair of this disorder is the Nissen fundoplication. This can be done from either an abdominal or transthoracic approach. When the procedure is done such that the gastric wrap is left above the diaphragm, serious complications can occur. These include gastric ulceration, gastric herniation with gastric outlet obstruction, slippage or perforation of the wrap, and gastrobronchial fistula. Because of these serious complications, the Nissen fundoplication with the wrap left above the diaphragm should only be used in certain situations, such as obesity and shortened esophagus.

Segmental wall motion abnormalities in an individual with idiopathic pulmonary hemosiderosis.

Idiopathic pulmonary hemosiderosis (IPH) is a rare condition characterized by diffuse pulmonary hemorrhage of unknown etiology. Cardiac involvement in the form of myocarditis and right ventricular hypertrophy have been reported to occur in association with IPH, although findings on echocardiography have not been described. Herein is presented a case of an adult with IPH and echocardiographic abnormalities.

Effect of stable fish oil on arterial thrombogenesis, platelet aggregation, and superoxide dismutase activity.

We examined the influence of dietary stable fish oil on aortic thrombosis, platelet aggregation, and superoxide dismutase (SOD) activity in a rat model. Twenty-nine Sprague-Dawley rats were fed regular chow supplemented with stable fish oil preparation (for 1 or 3 weeks), and 37 rats fed regular chow served as controls. The abdominal cavity was opened, and the abdominal aorta isolated. Whatman paper impregnated with 35% FeCl3 was wrapped around the surface of the aorta, and aortic flow was continuously recorded. In control rats, an occlusive platelet-fibrin-rich thrombus was formed in 21 +/- 3 min. Dietary fish oil in a time-dependent fashion delayed time to thrombus formation (24 +/- 2 min in rats fed fish oil for 1 week and 31 +/- 2 min in rats fed fish oil for 3 weeks), inhibited platelet aggregation (21 +/- 5% vs. 45 +/- 6%; p < 0.01) and increased SOD activity (p < 0.01). We conclude that dietary supplementation with stable fish oil delays formation of arterial thrombus, probably by reducing platelet aggregation and oxidative stress-associated arterial injury.