A distinctive cardiovascular lesion resembling histiocytoid (epithelioid) hemangioma. Evidence suggesting mesothelial participation

This paper presents 14 examples of a distinctive cardiovascular lesion. The patients' ages ranged from 5 to 76 years (mean, 51 years). There were seven male patients and seven female patients. All of the lesions were small and represented incidental surgical findings. Ten were attached to the endocardium, three were free-floating in the pericardial cavity, and one was inside a dissecting aneurysm of the ascending aorta. Microscopically, the lesions were enclosed in a fibrinous network and composed of a solid proliferation of round to polygonal cells with centrally located nuclei. Immunohistochemically, the cells were negative for FVIII-related antigen and lysozyme, but they stained positively for keratin, especially when clustered in small micropapillary or tubule-like formations. The nature and pathogenesis of these lesions are uncertain. Their location and some of their microscopic features originally suggested a relationship with the entity described as histiocytoid (epithelioid) hemangioma. However, their intense immunoreactivity for keratin, occasional presentation in the pericardial sac, and marked morphologic similarities with nodular mesothelial hyperplasia as sometimes seen in hernia sacs point toward the alternative possibility of a reactive mesothelial nature. A possible pathogenetic mechanism for the endocardial cases is ingrowth of pericardial mesothelial cells along a perforation tract that may have developed at the time of a cardiac catheterization. There were no recurrences or metastases in any of the cases.     

Causes of sudden death in athletes.

The incidence of sudden death in athletes is low. Some pathologic conditions, such as hypertrophic cardiomyopathy, coronary artery anomalies, and right ventricular dysplasia may predispose to sudden death during exercise in young athletes. In older individuals, exercise may trigger terminal arrhythmias in patients with atherosclerosis. Screening programs for young individuals undertaking athletic regimens are currently recommended only for those with a suggestive clinical or family history. For older individuals, caution should be advised for patients with known or suspected atherosclerotic disease.     

Cardiac damage induced by 2-amino-3-methyl-imidazo[4,5-f]quinoline in nonhuman primates.

The heterocyclic aromatic amine 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) is a potent hepatocarcinogen in cynomolgus and rhesus monkeys. The finding of high cardiac IQ-DNA adduct levels prompted a histopathological study of perfusion-fixed hearts from 10 tumor-bearing monkeys chronically dosed with IQ at 10 mg/kg or 20 mg/kg 5 days per week for 48-80 months. Two monkeys dosed only with the vehicle for IQ, hydroxypropylcellulose, served as controls. All the monkeys had normal heart weights, and no abnormalities were observed upon gross inspection of the hearts. Microscopically, focal myocardial lesions were observed in 8 of 10 monkeys dosed with IQ. Light microscopic abnormalities included myocyte necrosis with or without chronic inflammatory infiltrates, interstitial fibrosis with myocyte hypertrophy or atrophy, and vasculitis. Electron microscopic findings included disruption of the mitochondrial architecture (i.e., mitochondrial swelling and clearing of matrix densities), myofibrillar loss, disorganization of the normal alignment of sarcomeres, and occasional myocytes showing nuclear hypertrophy or peripheral clumping of the nuclear chromatin. There was some correlation between the cumulative dose of IQ and the extent of the myocardial abnormalities. These findings suggest that chronic exposure to IQ can lead to myocardial damage in monkeys. Although focal and not associated with clinical evidence of heart failure, these abnormalities may represent the initial stages of IQ-induced toxic cardiomyopathy.     

Neuroprotective effect of L-carnitine in the 3-nitropropionic acid (3-NPA)-evoked neurotoxicity in rats

A plant and fungal toxin, 3-NPA, acts as an inhibitor of mitochondrial function via irreversible inactivation of the mitochondrial inner membrane enzyme, succinate dehydrogenase (SDH). Inhibition of SDH disturbs electron transport and leads to cellular energy deficits and neuronal injury. We have shown that pretreatment with l-carnitine, while not significantly attenuating SDH inhibition, prevented hypothermia and oxidative stress-associated increased activity of free radical-scavenging enzymes. Here, a neurohistological method was applied to examine the effect of carnitine pretreatment against 3-NPA-induced neurotoxicity. Twenty adult male Sprague-Dawley rats were randomly divided into two groups (n = 10/group). Rats in the first group were injected twice with 3-NPA at 30 mg/kg s.c., 2 days apart, and the second group of animals received l-carnitine pretreatment at 100 mg/kg 30-40 min before 3-NPA administration. Rats in both groups were perfused 7 days later and their brains harvested. Degenerating neurons were identified and localized via the fluorescent marker Fluoro-Jade B. In the three animals that survived 3-NPA dosing, one exhibited no pathology, one exhibited moderate unilateral damage to the striatum, and the third exhibited extensive bilateral neuronal degeneration in multiple forebrain regions. In the seven surviving animals that received l-carnitine prior to 3-NPA insult, six exhibited no lesions, while one exhibited a modest unilateral lesion in the striatum. It appears that l-carnitine is protective against 3-NPA-induced toxicity, as reflected by both reduced mortality and significantly reduced neuronal degeneration.     

Percutaneous transluminal coronary angioplasty guidewire-induced coronary artery dissection without balloon inflation

A case of arterial dissection of the right coronary artery secondary to angioplasty guidewire manipulation is presented. No balloon inflation was performed. The histologic appearance of the involved arterial segment was similar to that found in the left anterior descending coronary artery, which had undergone successful balloon dilatation. Both arteries demonstrated medial disruption and fibrointimal proliferation. The pathologic features of angioplasty-induced vascular injury may occur with or without balloon inflation.     

Adult cellular rhabdomyoma of the heart: a report of 3 cases

We present 3 adults with cardiac rhabdomyomas, 2 in the atria and 1 in the right ventricle. One atrial tumor was discovered incidentally, and 1 resulted in supraventricular tachycardia. The ventricular lesion caused ventricular tachycardia. Compared with congenital rhabdomyomas, the tumors are relatively cellular, the cells are smaller, there are few spider cells, and there is evidence of cell proliferation. Two of the 3 tumors demonstrated spindling in contrast to adult rhabdomyomas of the head and neck. Although surgical excision was possible in all patients, long-term follow-up will be required to determine the true biologic behavior of these neoplasms.     

Stent design favorably influences the vascular response in normal porcine coronary arteries

OBJECTIVES: The purpose of this study was to compare the arterial response following implantation of a stainless-steel, balloon-expandable, tubular slotted stent with that of a novel computer-designed, multi-cellular stent in normal porcine coronary arteries. BACKGROUND: Intracoronary stent placement has evolved into the primary strategy for percutaneous revascularization of symptomatic coronary arterial lesions. Presently there is intense interest in developing new stent designs to improve stent delivery and biocompatability. METHODS: Computer-assisted design was utilized to develop a balloon-expandable stent with symmetric expansion properties, uniform arterial wall coverage, longitudinal flexibility and radial strength. Quantitative coronary angiography and histological assessment of the stented arteries was used to evaluate the acute and chronic vascular responses to a stainless-steel, balloon-expandable, tubular slotted stent as compared to the computer-designed BX stent in the normolipemic swine. RESULTS: Forty stents (24 BX, 16 tubular slotted) were implanted in 19 miniature swine at a mean inflation pressure of 9 atm using identical delivery systems. Eight of the BX and none of the tubular slotted stents were post-dilated with a non-compliant balloon at 12-14 atm. The mean stent-to-artery ratio was similar for the BX (1.03 +/- 0.06) and tubular slotted (1.04 +/- 0.11; p = 0.59) designs. Protrusion or asymmetric radial flaring of a strut at the stent margin was present in 1 of 23 BX stents (4.3%) and 10 of 15 tubular slotted stents (66.7%; p < 0.0001). The mean arterial injury score was significantly less for the BX stent (0.2 +/- 0.2) as compared with the tubular slotted stents (0.4 +/- 0.4; p = 0.025). At 3 days, thrombus area was similar for the BX and tubular slotted designs (0.42 +/- 0.16 mm2 versus 0.44 +/- 0.18 mm2, respectively; p = 0.88). The mean neointimal area was significantly less for the BX at 2 months (1.09 +/- 0.25 mm2 versus 2.93 +/- 2.26 mm2 in the tubular slotted stent) and at 6 months (1.10 +/- 0.26 mm2 versus 2.07 +/- 0.65 mm2 in the tubular slotted stent; p = 0.01), resulting in approximately 50% less in-stent stenosis. CONCLUSIONS: The arterial response to a balloon-expandable stent can be favorably influenced by computer-assisted modification of design in an experimental model. Further study is warranted to determine the impact of stent design upon clinical in-stent restenosis.