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Biomedical subjects

W D Edwards

Publications and source records attributed to W D Edwards.

At least 55 records · Page 3Linked to original sources
PubMed1997

Mechanical pressure and stretch release endothelin-1 from human atherosclerotic coronary arteries in vivo.

BACKGROUND: Endothelin-1 (ET-1) is an endothelium-derived vasoactive peptide with mitogenic properties. In vitro, vascular release of ET-1 is increased in response to mechanical stress. The goal of the present study was to examine whether ET-1 is released from human atherosclerotic coronary arteries in vivo in response to mechanical pressure and stretch and to characterize immunoreactivity for ET-1 and its precursor, big ET-1, within the atheromatous plaque. METHODS AND RESULTS: Circulating ET-1 levels were measured in 20 patients before and after coronary angioplasty for stable angina at three sampling sites: the femoral artery and the coronary artery segments proximal and distal to the lesion dilated. In addition, atheromatous tissue obtained from 20 patients undergoing directional coronary atherectomy for stable angina were analyzed for immunoreactivity for ET-1 and big ET-1. In patients undergoing angioplasty, ET-1 levels in the distal coronary artery increased after balloon dilatation (8.4 +/- 0.9 to 16.4 +/- 2 pg/mL, P < .05); proximal coronary artery and systemic ET-1 levels were unchanged. The degree of mechanical stress applied (product of duration and pressure of balloon inflation) correlated with the change in distal coronary artery ET-1 levels (r = .71, P < .01). Immunoreactivity for big ET-1 and ET-1 was ubiquitous in the extracellular space and the intracellular compartment (macrophages, myointimal cells, myofibroblasts, and endothelial cells) of human coronary atheromatous tissue. CONCLUSIONS: Big ET-1 and ET-1 immunoreactivity is ubiquitous within the intracellular and extracellular compartments of coronary atherosclerotic tissue. ET-1 is released from these sites in response to mechanical stress. These findings support a role for endothelins in the evolution and progression of coronary atherosclerosis in humans.

Aged↗
PubMed1997

Arterial remodeling after experimental percutaneous injury is highly dependent on adventitial injury and histopathology.

BACKGROUND: The extent and nature of unfavorable geometric remodeling, especially related to the adventitia, has not been studied previously. The purpose of this study was to examine two methods of experimental arterial injury, characterize the extent of remodeling, and determine if remodeling is injury-specific. METHODS: Two methods for producing coronary stenoses in pigs were used: heat injury using thermal balloon angioplasty (resulting in adventitial fibrosis), and copper stent implantation (resulting in intense inflammation). Histomorphometric parameters included changes in neointimal thickness (delta neointima) from uninjured to injured sections, and differences in area circumscribed by the internal and external elastic laminas (delta internal elastic lamina area and delta external elastic lamina area, respectively). Remodeling was calculated for each lesion as the enlargement of the external elastic lamina area or internal elastic lamina area for incremental neointimal thickening, expressed as the slopes delta external elastic area/delta neointima and delta internal elastic lamina area/delta neointima. RESULTS: Remodeling indices for the heat lesions for the heat lesions were negative (delta internal elastic lamina area/delta neointima = 0.15, delta external elastic lamina area/delta neointima = 0.64) and indicated little remodeling in contrast to copper stent injury (delta internal elastic lamina area/delta neointima = 0.95, delta external elastic lamina area/delta neointima = 1.20). CONCLUSIONS: Remodeling in fibrotic compared to inflammatory lesions differs markedly, and may explain increased restenosis rates observed in thermal balloon angioplasty in patients. This formulation may be useful to study remodeling and restenosis following interventional technologies.

Angioplasty, Balloon, Coronary↗
PubMed1997

Short wave ultraviolet laser energy in porcine coronary arteries: medial cell death and neointimal formation.

BACKGROUND AND OBJECTIVE: Smooth muscle cell migration and proliferation from arterial media into the neointima are major factors in the restenosis process following coronary angioplasty. Because short wave ultraviolet (UV) radiation is cytotoxic for rat carotid artery smooth muscle cells, the aims of this study were to determine the effects of short wave UV irradiation on normal pig coronary arteries and to evaluate the efficacy of UV laser energy for reducing neointimal hyperplasia (NI). STUDY DESIGN/MATERIALS AND METHODS: In 13 pigs fed a normal diet, 37 coronary arteries were studied. UV laser light (275 nm) was applied in escalating doses from 0-16,353 mJ/cm2 via fiberoptic through a 20 mm PTCA balloon catheter. The pigs were euthanized at 21 days and histologic analysis performed. Arterial media was rendered acellular (ACM) in 20 of 33 irradiated coronary arteries (61%). The minimum UV energy density inducing ACM was 1348 mJ/cm2. The fraction of acellular media to internal elastic lamina length (ACM/IEL) was 0.79 +/- 0.29. RESULTS: No statistically significant difference was found between NI thickness at normal media sites (NM) vs. ACM sites (0.17 +/- 0.14 mm vs. 0.16 +/- 0.17 mm). No correlation was found between UV dose and NI formation (r = 0.307, P = 0.08). CONCLUSION: Short wave UV irradiation induces ACM in normal porcine coronary arteries. Induction of acellular media is not associated with a reduction of NI formation in this porcine coronary model.

Angioplasty, Balloon, Coronary↗
PubMed1997

Calcified amorphous tumor of the heart (cardiac CAT).

Eleven cases of poorly characterized nonneoplastic endocardially based intracavitary cardiac masses have been seen at the Mayo Clinic between 1965 and 1994. They occurred in 7 women and 4 men from age 16 to 75 years (mean, 52 years). The patients presented with a wide variety of symptoms and underlying diseases. The lesions were diagnosed as a primary cardiac neoplasm in 6 of 8 patients having echocardiography. Surgical excision was the treatment of choice in 10 patients; the 11th patient died of noncardiac causes 30 days after the mass was discovered. Grossly, the lesions were firm, yellow-white, and partially calcified, and arose in any of the four chambers. Microscopically, all lesions were characterized by nodular calcium in a background of degenerating blood elements and chronic inflammation. All patients had a benign course relative to their cardiac lesion. Repeat echocardiogram in two patients showed residual calcium in the region of the initial tumor. Although these lesions may represent calcified thrombi, the clinical presentation did not suggest thrombosis as the most likely explanation for their occurrence. Based on the combined clinical presentation and microscopic appearance, the authors propose the descriptive name calcified amorphous tumors (cardiac CAT) to describe this group to nonneoplastic cardiac masses.

Adolescent↗
PubMed1997

Histologic correlates of angiographic chronic total coronary artery occlusions: influence of occlusion duration on neovascular channel patterns and intimal plaque composition.

OBJECTIVES: Age-related changes in histologic composition and neovascular channel (NC) pattern of angiographic chronic total coronary artery occlusions (CTOs) were studied to define histologic correlates of age-related revascularization profiles and neovascular channel formation. BACKGROUND: Revascularization of CTOs is frequently characterized by inability to cross or dilate the lesion and a high incidence of reocclusion or restenosis but low periprocedural ischemic complication rates. Little is known about the histopathologic basis of these observations. METHODS: Ninety-six angiographic CTOs from autopsy studies in 61 patients who had undergone coronary angiography within 3 months of death were studied. Abrupt plaque rupture was excluded. Occlusion segments were analyzed for 1) histologic composition as a function of lesion age; and 2) NC pattern as a function of lesion age and intimal plaque (IP) composition. RESULTS: Cholesterol and foam cell-laden IP was more frequent in younger lesions (p = 0.0007), whereas fibrocalcific IP increased with CTO age (p = 0.008). IP NCs arose directly from adventitial vasa vasorum and were anatomically and quantitatively related in terms of number and size (p = 0.0001) to the extent of IP cellular inflammation. IP cellular inflammation exceeded that found in the adventitia (p < 0.001) or media (p = 0.0001) across all CTO ages. In CTOs < 1 year old, the adventitia was associated with a larger number and size of NCs relative to the IP (p = 0.0006 and p = 0.009), media (p = 0.0001 and p = 0.002) and recanalized lumen (p = 0.0001 and p = 0.001). In CTOs >1 year old, the adventitia and IP NC numbers were similar and exceeded NC numbers found in the media (p = 0.0001) and recanalized lumen (p = 0.0001 and p = 0.003). CONCLUSIONS: Angiographic CTO frequently corresponds to less than complete occlusion by histologic criteria. Age-related changes in IP composition from cholesterol laden to fibrocalcific may explain the adverse revascularization profile of older CTOs. IP NC growth derived from the adventitia increases with age and is strongly associated with IP cellular inflammation. IP NC formation may protect against the flow-limiting effects of IP growth.

Adult↗
PubMed1997

Papillary fibroelastoma: echocardiographic characteristics for diagnosis and pathologic correlation.

OBJECTIVES: We sought to determine the clinical and echocardiographic characteristics of papillary fibroelastoma (PFE). BACKGROUND: PFE is a rarely encountered cardiac tumor about which relatively little is known. METHODS: Institutional records were reviewed for the years 1980 to 1995 for patients with pathologic or echocardiographic diagnosis of PFE. Group 1 included 17 patients with the pathologic diagnosis of PFE who also underwent echocardiography. Echocardiographic features of PFE were established in group 1. Group 2 included 37 patients with only echocardiographic evidence of PFE. RESULTS: In group 1, 7 (41.2%) of 17 patients had symptoms related to PFE. Neurologic events occurred in 5 (29.4%) of 17 patients. All patients had the tumor surgically removed. During follow-up, no new embolic events occurred. Echocardiographic characteristics of PFE included a small tumor (12.1 +/- 6.5 x 9.0 +/- 4.3 mm), usually pedunculated (14 [94%] of 17 patients) and mobile, with a homogeneous speckled pattern and a characteristic stippling along the edges. PFEs were most common on valvular surfaces (12 [60%] of 20 PFEs) but were not uncommon on other endocardial surfaces (8 [40%] of 20 PFEs). The tumor did not cause valvular dysfunction. In group 2, 16 (43%) of 37 patients were asymptomatic. Five patients (13.5%) had a previous neurologic event. During follow-up (mean 31 months, range 1 to 77), nine neurologic events occurred. CONCLUSIONS: PFEs are associated with embolism, can be diagnosed with echocardiography, are often an incidental clinical finding and do not cause valvular dysfunction.

Endocardium↗
PubMed1997

Acute myocardial infarction followed by technetium-99m-sestamibi SPECT imaging and pathologic correlation.

A 79-yr-old man received thrombolytic therapy for acute myocardial infarction after injection with 99mTc-sestamibi and died shortly thereafter. Postmortem in situ SPECT imaging of the heart was performed. The heart was then removed and sectioned into short-axis slices, which were placed directly on the SPECT camera face for imaging, and examined by routine gross and microscopic pathologic methods. Pathologic findings were consistent with a small acute inferoseptal myocardial infarction, as demonstrated on both SPECT imaging of the intact heart and imaging of the heart slices. This case report provides further evidence of the validity of SPECT sestamibi imaging for the determination of myocardium at risk during acute myocardial infarction.

Aged↗
PubMed1996

Relationship of vascular thrombosis and inflammatory leukocyte infiltration to neointimal growth following porcine coronary artery stent placement.

BACKGROUND: Superficial and intramural thrombosis are reproducible histopathological features of the porcine coronary oversized stent injury model. Fibrin and its degradation products are chemotactic for mononuclear leukocytes, and promote the proliferation and migration of vascular smooth muscle cells (VSMC) in vitro. The goal of this study was to quantitate the serial histomorphologic evolution of thrombosis, leukocyte infiltration, VSMC proliferation and collagen accumulation following porcine coronary artery stent placement in a porcine model. METHODS: Twenty-four normocholesterolemic swine underwent oversized balloon (3.5-4.0 mm) coronary angioplasty and tantalum metal stent placement. Twenty-six different arterial sites were injured, followed by serial sacrifice at day 4 (n = 6), 8 (n = 6), 14 (n = 6), and 28 (n = 6). Quantitative analysis of the neointima was performed using a high resolution video-microscopy interface and a validated histomorphometric software program. Alpha actin-positive VSMC density (per 10(4) micro(2) neointimal area) and collagen-specific picro-sirius red fluorescence (percent of neointima) were quantitated at sites adjacent to and distant from coronary artery stent placement. RESULTS: The percent of total neointimal area occupied by resolving thrombus material was greater at days 4-8 compared to 14-28 days (59-63% vs. 1-2%; P = 0.001). Mononuclear leukocytes were also significantly increased at days 4 and 8 (92 +/- 1 and 70 +/- 8%) compared to days 14-28 (both 3 +/- 3%; P = 0.001), as a percentage of the total neointimal cellularity. Total neointimal cell density did not change (20 +/- 10, 12 +/- 6, 23 +/- 7 and 20 +/- 3 cells/10(4) micro(2); P-value, NS), despite progressive cross-sectional vascular area stenosis reduction from 7 +/- 3% at day 4 to 72 +/- 14% at day 28 (P = 0.001). Percent neointimal fibrinoid thrombus content and mononuclear leukocyte cellularity were correlated in this model (R = 0.81; P < 0.001). Peri-stent neointimal collagen staining exceeded that at vascular sites distant from porcine coronary stent placement by 14 days (29 +/- 6 vs. 15 +/- 3%), and remained greater at 28 days (35 +/- 11 vs. 16 +/- 12%) (both P < 0.05). CONCLUSIONS: Quantitative serial histomorphometry of porcine coronary vascular stent delivery sites demonstrates early (4-8 day) neointimal mononuclear leukocyte infiltration which is histomorphologically and temporally related to intramural fibrinoid thrombosis. Significant vascular stenosis and collagen deposition occurs by 14-28 days at these vascular injury sites. These data suggest a local interaction between thrombotic and inflammatory elements in porcine coronary neointima following oversized stent injury.

Angioplasty, Balloon↗
PubMed1996

Two unusual variants of internal carotid artery aneurysms due to fibromuscular dysplasia.

Aneurysms of the internal carotid artery (ICA) secondary to fibromuscular dysplasia (FMD) are extremely rare. We report two unique variants of extracranial ICA aneurysms due to FMD. The first patient was a hypertensive 51-year-old woman who was found to have a nontraumatic, nonmycotic saccular pseudoaneurysm of the right ICA. The second patient was a 46-year-old woman who presented with 90% stenosis and a focal dissecting aneurysm of the right ICA. Both underwent successful aneurysm resection with interposition saphenous vein grafting after anterior subluxation of the mandible. A review of the literature revealed only 21 other reported cases of aneurysms of the extracranial ICA due to FMD; all were managed successfully with surgical repair. Surgery can be performed with minimal or no morbidity, even in the distal ICA, if the exposure is adequate.

Aneurysm↗
PubMed1996

Thoracoscopic obliteration of the left atrial appendage: potential for stroke reduction?

BACKGROUND: In a review of all relevant articles describing the site of left atrial thrombus in patients with atrial fibrillation, the thrombus was localized to the left atrial appendage in 43% of patients with rheumatic heart disease and in 91% of patients with nonrheumatic atrial fibrillation. This study was designed to test the feasibility of thoracoscopic obliteration of the left atrial appendage as a means of reducing thromboembolic stroke. METHODS: Thoracoscopic obliteration of the left atrial appendage was undertaken in 10 dogs, 5 with staples and 5 with an endoloop. Obliteration also was attempted in 8 fresh human cadavers. RESULTS: In all dogs, the appendage was rapidly obliterated (21.3 +/- 7.6 minutes) and confirmed at euthanasia at 11 weeks. In 3 cadavers, anatomic and disease factors prevented visualization of the left atrial appendage; in 1 the appendage tore, and in the remainder the appendage was obliterated. CONCLUSIONS: Obliteration of the left atrial appendage is feasible and may be considered as an additional surgical procedure to reduce stroke. The group of patients in whom it offers the greatest potential are those with atrial fibrillation deemed ineligible for warfarin, those without atrial thrombus and with a free pericardial and pleural space.

Animals↗
PubMed1996

A proliferation analysis of arterial neointimal hyperplasia: lessons for antiproliferative restenosis therapies.

Medial smooth muscle cell proliferation is frequently implicated as the major cause of coronary restenosis. Although antiproliferative agents have shown efficacy in animal studies, they are ineffective in human trials. To better understand these discrepancies, we performed a mathematical kinetic analysis of cellular proliferation in the neointimal hyperplasia of rats, pigs, and patients. A model was derived using a differential expression for proliferation, proportional to the number of cells present. Additional terms were included for inhibition of proliferation proportional to neointimal mass and time. The resulting equation was solved in closed form for the number of cells and proliferation rate. These equations were validated in the rat carotid artery injury model from published data. The model was then applied to the porcine coronary injury model, and then to clinical data obtained from angiographic human studies. Peak cellular proliferative activity in patients occurs at 16 days and continues at lower levels for much longer periods of time. Less than 10 generations of cells are sufficient to develop clinically significant restenosis. Conversely, proliferation rates in the two animal models (rats and pigs) are maximal at roughly 2 and 6 days, respectively, also continuing at low levels for extended time periods. Cell proliferation in restenosis is a highly controlled process, with comparatively few cell generations causing enough neointima for arterial obstruction to occur. Substantial cell kinetic differences occur across species. The rat exhibits high proliferation rates and rapid doubling times compared to patients and pigs, and is thus a highly 'proliferative' model. Such differences may be responsible for discrepant animal model and clinical trial results. These data may help determine the timing and strategy of therapy against clinical restenosis.

Animals↗
PubMed1996

The premortem recognition of systemic senile amyloidosis with cardiac involvement.

PURPOSE: To recognize systemic senile amyloidosis involving the heart and to determine outcome. PATIENTS AND METHODS: All patients with the diagnosis of amyloidosis at the Mayo Clinic from January 1, 1984 through May 1, 1992, were reviewed. Amyloid was confirmed histologically by sulfated alcian blue and alkaline Congo red staining. The labeled streptavidin-biotin immunoperoxidase method was used with antisera against A kappa, A lambda, AA, transthyretin, and beta 2-microglobulin. Anti-P-component and antisera to albumin were used as controls. Chest radiographs, electrocardiograms, transthoracic echocardiograms, and cardiac catheterization data of all patients were reviewed. Serum and urine were examined with immunoelectrophoresis and immunofixation for the presence of a monoclonal protein. Lymphocyte DNA was examined for transthyretin mutations associated with familial amyloidosis. RESULTS: We identified 18 patients with myocardial tissue that stained positive for amyloid with sulfated alcian blue and Congo red and with transthyretin antisera. Congestive heart failure was present at diagnosis in 17 of the 18 patients. Atrial fibrillation was found in 11 patients. No monoclonal protein was found in the serum or urine. The echocardiographic findings were consistent with infiltrative cardiomyopathy due to amyloidosis in 16 patients. Right heart pressures were elevated in all 7 patients who had right-side heart catheterization. No transthyretin mutations were found in the leukocyte DNA from 12 patients. The actuarial median survival was 5 years; in contrast, the median survival was 5.4 months in 147 patients with primary amyloidosis (AL) who presented with congestive heart failure. CONCLUSION: Patients with cardiac amyloid and no monoclonal protein in the serum or urine must have immunohistochemical staining for kappa and lambda light chains and transthyretin to distinguish between systemic senile amyloidosis, familial amyloidosis, and AL. Patients with systemic senile amyloidosis should not be treated with alkylating agents. Their survival is much longer than that of patients with AL (60 versus 5.4 months).

Age Factors↗
PubMed1996

Pathology of radiation-induced heart disease: a surgical and autopsy study of 27 cases.

During the 20 years between 1973 and 1992, 27 patients were identified in whom cardiac tissue was available (15 surgical, 10 autopsy, and 2 both) that exhibited radiation-related injury. Specimens were assessed for damage to the pericardium, valves, myocardium, and coronary arteries. Patients ranged in age from 22 to 76 years (mean, 49 years), and 19 were men. Among 20 cases with available pericardium, 14 (70%) had radiation-related disease including six with an effusion, three with constriction, two with both, and three with neither. In 17 cases with available valves, 12 (71%) showed radiation injury involving 25 valves (nine mitral, eight aortic, five tricuspid, and three pulmonary), although clinically significant dysfunction was diagnosed in only eight. For the 16 patients from whom myocardium was available, 10 (63%) exhibited radiation-related fibrosis, which was moderate or severe in only the seven who received more than 3,000 rad (cGy). Among the 13 cases with available coronary arteries, only two had unequivocal radiation-induced obstructions (26- and 44-year-old men with Hodgkin's disease). In conclusion, radiation injury to the heart includes not only constrictive pericarditis and myocardial fibrosis, but also appreciable valvular and coronary artery lesions. As patients with malignancies survive longer, the surgical relief of radiation-induced heart disease may become more prevalent.

Adult↗
PubMed1996

Pulmonary venoocclusive disease: CT findings in eight patients.

OBJECTIVE: The objective of the study was to describe the CT findings of pulmonary venoocclusive disease. MATERIALS AND METHODS: Eight patients with CT scans of the thorax and a diagnosis of pulmonary venoocclusive disease were identified from three institutions. The six males and two females had a mean age of 32 years old (range, 5-58 years old). All scans were evaluated with consensus reading by two chest radiologists. Lung parenchyma were assessed for the type and distribution of disease. Bronchi, pleura, hila, mediastina, and chest walls were evaluated for abnormalities. Pathologic specimens from five patients were reviewed and specifically correlated with the radiologic findings. RESULTS: Seven of the eight patients had interlobular septal thickening. All eight patients had regions of ground-glass opacity. Four of the eight patients had a mosaic pattern of lung attenuation. No enlarged hilar or mediastinal nodes were revealed. Five patients had bilateral pleural effusions. CONCLUSION: The most common CT findings in these eight patients with pulmonary venoocclusive disease were smooth interlobular septal thickening, diffuse multifocal regions of ground-glass opacity, pleural effusions, enlarged central pulmonary arteries, and pulmonary veins of normal caliber. Four patients had a mosaic pattern of lung attenuation on the CT scans. These findings are highly suggestive of pulmonary venoocclusive disease and may be helpful in difficult cases. Definitive diagnosis requires lung biopsy.

Adolescent↗
PubMed1996

The effects of lovastatin on neointimal hyperplasia following injury in a porcine coronary artery model.

OBJECTIVE: To assess the effectiveness of lovastatin, an HMGCoA reductase inhibitor, in the inhibition of coronary arterial restenosis post-balloon angioplasty. DESIGN: Randomized single-blind study comparing the degree of restenosis in a control and lovastatin group of animals with similar degree of arterial injury. ANIMALS: Seventeen domestic cross-bred pigs received either oral lovastatin (11 animals) or no lovastatin (six animals). INTERVENTIONS: The pigs received 20 mg of oral lovastatin twice daily or no drug. All pigs received acetylsalicylic acid and verapamil preprocedure. One or more coronary arteries were injured by deployment of tantalum wire stents delivered on oversized percutaneous transluminal coronary angioplasty balloons. The balloons were intentionally overexpanded to create arterial injury. The animals were sacrificed at 28 days. The arteries were cross-sectioned and evaluated blindly by quantitative histomorphometry. The amounts of arterial injury and neointimal thickening were quantitated. A series of linear regression models was used to control for the degree of injury. MAIN RESULTS: The reduction of neointimal thickness for the lovastatin group compared with the control animals was 0.08 mm, a statistically significant result (P < 0.05). CONCLUSIONS: Although lovastatin produced a statistically significant decrease in neointimal thickness post-balloon angioplasty, when extrapolated to angiographical end-points, the differences would not be clinically significant. These data suggest that lovastatin may be of marginal use in humans for limiting restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1995

Tuberous sclerosis and cardiac rhabdomyoma.

We conclude that echocardiographically detected cardiac rhabdomyomata are common in patients with tuberous sclerosis complex, and are more prevalent and prominent in the younger patient. Tumors regress in size or number, or both, in most patients aged < 4 years, and less so in older patients. Cardiac rhabdomyomata are associated with a higher incidence of preexcitation and may increase the risk for arrhythmia.

Adolescent↗
PubMed1995

Sudden unexpected nontraumatic death in 54 young adults: a 30-year population-based study.

The objective of this study was to evaluate the incidence and correlates of sudden unexpected nontraumatic death among young adults in a well-surveyed population. The incidence and pathogenesis of sudden unexpected nontraumatic death in a young adult population (aged 20 to 40 years old) have not been well defined. All residents 20 to 40 years old from Olmsted County, Minnesota, who had nontraumatic sudden death between 1960 and 1989 were included. Histologic and gross cardiac specimens were examined. The incidence of sudden death was estimated based on the ratio of number of observed events to relative census data for the Olmsted County population from the last 3 decades. Statistical comparisons between age decades were obtained with the chi-square test. Incidence trends were tested using Poisson regression. Of the 54 subjects, 19 were women (4.1/10(5) population annually) and 35 were men (8.7/10(5) population annually). An increase in incidence of sudden death was evident in men. Causes of death included coronary artery disease, noncardiovascular disease, suspected primary arrhythmia, vascular disease, myocarditis, hypertrophic cardiomyopathy, and unknown causes. Gross and histologic features suggestive of right ventricular dysplasia were found in 9 subjects (17%), but 6 of these 9 had other established causes of death. Of the 27 sudden deaths between 1980 and 1989, 9 (33%) had a history of cocaine abuse. A trend in increasing incidence of sudden death in young men is noted. A high prevalence of cocaine abuse was observed in young adults who died suddenly. Histologic features of right ventricular dysplasia were prevalent but were not necessarily the primary cause of death.

Adult↗