Lifetime risk estimation for cardiovascular disease (CVD) has been proposed as a useful strategy to improve risk communication in the primary prevention setting. However, the perception of lifetime risk for CVD is unknown. We included 2,998 individuals from the Dallas Heart Study. Lifetime risk for developing CVD was classified as high (≥39%) vs. low (<39%) according to risk factor burden as described in our previously published algorithm. Perception of lifetime risk for myocardial infarction was assessed via a 5-point scale. Baseline characteristics were compared across levels of perceived lifetime risk. Multivariable logistic regression analyses were performed to determine the association of participant characteristics with level of perceived lifetime risk for CVD and with correctness of perceptions. 64.8% (1942/2998) of participants were classified as high predicted lifetime risk for CVD. There was significant discordance between perceived and predicted lifetime risk. After multivariable adjustment, family history of premature MI, high self-reported stress, and low perceived health were all strongly associated with high perceived lifetime risk (OR [95% CI]: 2.37 [1.72–3.27], 2.17 [1.66–2.83], and 2.71 [2.09–3.53]). However, the association between traditional CVD risk factors and high perceived lifetime risk was more modest. In conclusion, misperception of lifetime risk for CVD is common and frequently reflects the influence of factors other than traditional risk factor levels. These findings highlight the importance of effectively communicating the significance of traditional risk factors in determining the lifetime risk for CVD.
BackgroundPheochromocytomas and Paragangliomas (PCC/PGL) are rare endocrine tumors that are mostly benign, but often hormone producing, causing significant morbidity and mortality due to excess catecholamine secretion and cardiovascular crises. It is estimated that 30% of PCC/PGL are due to germline mutations, including Neurofibromatosis type 1 (NF1). There is little published data describing the phenotype of NF1-associated PCC/PGL and there are no established recommendations for PCC/PGL screening in NF1.MethodsWe conducted a retrospective chart review of 17 patients with NF1-associated PCC/PGL who received care at a large academic referral center between the years of 1992–2016.ResultsAverage age of diagnosis was 42 years old. Both genders were equally affected. Average tumor size was 3.9 cm. Nine patients were hypertensive; one had orthostatic hypotension; three had tachycardia; the remaining two patients had normal BP and HR. Most tumors were benign, unilateral adrenal tumors that were hormonally active. Two had metastatic disease. Six patients experienced cardiovascular crises; three of which occurred during elective surgeries for neurofibroma removal, and a fourth occurred during labor and delivery.ConclusionThese data highlight the importance of screening for PCC/PGL in NF1, especially prior to surgical procedures and pregnancy, labor and delivery as these events can trigger a cardiovascular crisis. Screening is easily accomplished with plasma or urine free fractionated metanephrine levels.Electronic supplementary materialThe online version of this article (10.1186/s40842-018-0065-4) contains supplementary material, which is available to authorized users.
Introduction: Patients with familial hypercholesterolemia (FH) suffer from premature coronary heart disease (CHD) due to extreme elevations in low-density lipoprotein cholesterol (LDL-C). As such, they require high doses of potent statins, a major risk factor for developing statin-induced myopathy. Little is known, though, about other underlying factors predisposing them to statin-induced myopathy. Methods: We studied 272 genetically screened FH patients - ascertained from Dallas, TX, lipid specialty clinics - with and without a documented history of statin-induced myopathy (defined as developing muscle symptoms or elevated serum creatine kinase (CK) levels while taking a statin). Results: Statin-induced myopathy was diagnosed in 35% of FH patients; however, at the time of participation in our study, 73% of myopathy patients were taking statins (vs 79% of statin-tolerant patients; p = 0.37). Statin dosages were similar in the two groups except for rosuvastatin (20 mg/day in myopathy patients vs 40 mg/day in statin-tolerant patients; p < 0.001). Myopathy patients were older (57 ± 11 vs 51 ± 14 years; p = 0.001), had lower BMI (29 ± 6 vs 31 ± 7 kg/m2; p = 0.01), suffered from less premature CHD (22% vs 34%; p = 0.006), and had less hypertension (57% vs 67%; p = 0.05). On-treatment LDL-C was higher in myopathy patients (141 ± 37, n = 63, vs 128 ±40 mg/dL, n= 148; p < 0.01). No differences were identified in pretreatment LDL-C (253 ± 53 vs 263 ± 83 mg/dL; p = 0.57), gender (63% vs 57 % female; p = 0.3), % with diabetes (23% vs 29%; p = 0.38), % with LDL-receptor or apolipoprotein B mutations (26% vs 36%; p = 0.09), or baseline CK levels (median 103 vs 115; p = 0.10). Conclusions: Despite a history of statin-induced myalgia, most FH patients eventually tolerated statins and achieved up to 44% reduction in LDL-C levels. FH patients with increased age and lower BMI were more likely to be diagnosed with myopathy, consistent with prior reports that age and smaller body frame are risk factors. Also, FH patients lacking hypertension or premature CHD were diagnosed more often with myopathy, suggesting that patients without CHD risk factors complain more about muscle symptoms. In conclusion, statin-induced myopathy adds an additional - but manageable - challenge to the treatment of FH patients.
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