Favorable cardiovascular risk profile and 10-year coronary heart disease incidence in women and men: results from the Progetto CUORE.

BACKGROUND: Cardiovascular risk factor research has recently broadened its focus based on new data indicating the benefits of low risk, i.e. favorable levels of all major risk factors. The aims of this study were to assess further the relation of low risk to coronary heart disease risk, and implications for prevention. DESIGN: We conducted a prospective population-based Italian study, of 7438 men and 13 009 women aged 35-69 years, with a mean follow-up of 10.4 years and validated first coronary events. METHODS: Baseline coronary heart disease risk was classified into three categories: low risk; unfavorable but not high risk; and high risk. To analyze the relation of these risk profiles to coronary heart disease incidence, age-adjusted, sex-averaged coronary heart disease incidence was calculated for persons free of coronary heart disease and stroke, stratified as baseline low risk, unfavorable but not high risk or high risk. To assess the independent relationship of individual risk factors to coronary heart disease incidence, multivariate proportional hazards models were computed for combinations of risk factors. RESULTS: Only 2.7% of participants met low risk criteria; 81.4% were high risk. Age-adjusted coronary heart disease incidence for the whole cohort was 37.1 out of 10000 person-years (men 59.0; women 15.3). No coronary heart disease events occurred in low-risk men, only two in low-risk women. For women and men who were not high risk, the age-sex standardized coronary heart disease rate was 62% lower than for high-risk participants. Blood pressure, need for antihypertensive medication, smoking, hyperglycemia, diabetes, total and high-density lipoprotein cholesterol were independently related to coronary heart disease risk. CONCLUSIONS: Favorable levels of all modifiable readily measured risk factors - rare among Italian adults - assure minimal coronary heart disease risk. Population-wide prevention is needed, especially improved lifestyles, to increase the proportion of the population at low risk.     

Respiratory Muscle Overloading and Dyspnoea During Bronchoconstriction in Asthma: Protective Effects of Fenoterol

Whether, and to what extent, β₂-agonists protect against respiratory muscle overloading and breathlessness during bronchoconstriction remains to be defined in patients with asthma. In a double blind placebo-controlled study, 100 μg of fenoterol were administered to six stable asthmatics before a bronchial provocation test, performed by inhaling doubling concentrations of histamine from a Devilbiss 646 nebulizer. We recorded breathing pattern (tidal volume V_T, inspiratory time T_I, total time of the respiratory cycle T_TOT), inspiratory capacity (IC), dynamic pleural pressure swing (P_plsw), total lung resistance (R_L) and FEV₁. V_Twas expressed both in actual values and as % of IC. Changes in V_T(%IC) during histamine inhalation reflected changes in dynamic end-inspiratory lung volume (EILV). P_plswwas expressed as % of maximal (the most negative in sign) pleural pressure, obtained under control conditions during a sniff manoeuvre (P_plsn). P_plsw(%P_plsn) is an index of inspiratory muscle effort. The test ended when the concentration of histamine which caused a decrease in FEV₁of ≥40% post-saline was reached. Dyspnoea rating was scored by a modified Borg scale. At the ultimate degree of bronchoconstriction (UDB) with histamine: (i) decrease in FEV₁was similar after placebo and fenoterol, while increase in R_Lwas lower after fenoterol (P<0.005); (ii) V_T(%IC) increased less after fenoterol (P<0.027); (iii) increases in P_plsw(%P_plsn) was lower after fenoterol (P<0.001); (iv) ΔBorg (from saline) was lower (P<0.01) after fenoterol; (v) differences in ΔBorg, from placebo to fenoterol, related to concurrent changes in V_T(%IC) (r²=0.67). In conclusion, at UDB 100 μg of fenoterol produced a beneficial effect on the degree of inspiratory muscle loading and breathlessness, an effect greater than it would be expected from measuring FEV₁alone.     

To fix or not to fix? The role of fibular fixation in distal shaft fractures of the leg

Background

The role of stabilisation of the fibula in distal two-bone fractures of the leg is controversial. Some studies indicate the need for fibular stabilisation in 43 AO fractures, but few studies consider the role of the fibula in 42 AO fractures. The aim of the current paper is to explain the role of stabilisation of the fibula in 42 AO fractures, correlating the rates of healing and non-union between patients with and without fibula fixation.

Materials and methods

A total of 60 patients with 42 AO (distal) shaft fracture of the tibia with associated fracture of the fibula were selected. Patients were divided into two groups according to whether or not the fibula was fixed: Group I (n = 26) comprised patients who had their fibula fixed while Group II (n = 34) comprised patients who did not. The fibular fracture was classified according to the AO and related to the level of the tibial fracture. Other parameters examined were the union rate of the two groups correlated to the fracture pattern and position of the fibular fracture; the demographic data, such as age and gender; the presence of an open fracture, and the type of tibial fixation device used (nail or plate).

Results

None of the parameters considered (open injury, AO classification, device used and level of the fibular fracture relative to the tibial) were shown to have an influence on the development of a non-union.

Conclusion

This study showed a higher non-union rate when the fracture of the tibia and fibula were at the same level, the tibia was fixed with a bridging plate and the fibula left untouched. For this reason, we recommend fibular fixation in all 42 distal fractures when both fractures lie on the same plane and the tibial fracture is relatively stabilised.     

Hypertrophic Cardiomyopathy : Present and Future,With Translation Into Contemporary Cardiovascular Medicine

Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with diverse phenotypic and genetic expression, clinical presentation, and natural history. HCM has been recognized for 55 years, but recently substantial advances in diagnosis and treatment options have evolved, as well as increased recognition of the disease in clinical practice. Nevertheless, most genetically and clinically affected individuals probably remain undiagnosed, largely free from disease-related complications, although HCM may progress along 1 or more of its major disease pathways (i.e., arrhythmic sudden death risk; progressive heart failure [HF] due to dynamic left ventricular [LV] outflow obstruction or due to systolic dysfunction in the absence of obstruction; or atrial fibrillation with risk of stroke). Effective treatments are available for each adverse HCM complication, including implantable cardioverter-defibrillators (ICDs) for sudden death prevention, heart transplantation for end-stage failure, surgical myectomy (or selectively, alcohol septal ablation) to alleviate HF symptoms by abolishing outflow obstruction, and catheter-based procedures to control atrial fibrillation. These and other strategies have now resulted in a low disease-related mortality rate of <1%/year. Therefore, HCM has emerged from an era of misunderstanding, stigma, and pessimism, experiencing vast changes in its clinical profile, and acquiring an effective and diverse management armamentarium. These advances have changed its natural history, with prevention of sudden death and reversal of HF, thereby restoring quality of life with extended (if not normal) longevity for most patients, and transforming HCM into a contemporary treatable cardiovascular disease.     

The Association between Cognitive Impairment and Diabetic Foot Care: Role of Neuropathy and Glycated Hemoglobin

Diabetes mellitus is associated with impairment in cognitive functions which can complicate adherence to self-care behaviors. We evaluated the incidence of cognitive impairment in patients with diabetes mellitus to determine the strength of the association between diabetic foot (a complication that occurs in about 10% of diabetic patients), adherence to the clinician’s recommendations, glycemic control, and cognitive function. A prospective study was carried out in a probabilistic sample of older patients with diabetic foot living in three nursing homes. Cognitive functions were evaluated by the MMSE (Mini-Mental State Examination), the Trail Making test (TMT), and the Michigan neuropathy screening instrument (MNSI). There were no significant associations between cognitive function and neuropathy or foot alterations, although glycated hemoglobin (HB1Ac > 7%) significantly (p < 0.05) associated with MMSE and adherence to treatment in the 1 month follow-up visit. Receiver operating characteristic curve analysis showed that both HB1Ac and the MNSI score significantly (p < 0.05) discriminate subsequent adherence to treatment for foot complication, with a sensitivity of 80.0–73.3% and specificity 70.6–64.7%, respectively. Proper control of foot complications in diabetic patients involves appropriate glycemic control and less severe neuropathy, and seems to be unrelated to cognitive dysfunction, and warrants further studies in order to tailor appropriate treatments to central and peripheral nervous system disorders. Poor glycemic control (Hb1Ac level > 7%) and a neuropathy score of 5.5 in the MNSI are the best-cut off points to discriminate poor adherence to the clinician’s recommendations for self-care behaviors in people with diabetic foot complication. In this study, we observed that foot disorders were associated with impaired global cognitive function in elderly patients (aged ≥ 65). Podiatrists and physicians should consider cognitive dysfunction as an important chronic complication in the management of diabetic foot.     

Pharmacological treatment of hypertrophic cardiomyopathy: current practice and novel perspectives

Hypertrophic cardiomyopathy (HCM) is entering a phase of intense translational research that holds promise for major advances in disease‐specific pharmacological therapy. For over 50 years, however, HCM has largely remained an orphan disease, and patients are still treated with old drugs developed for other conditions. While judicious use of the available armamentarium may control the clinical manifestations of HCM in most patients, specific experience is required in challenging situations, including deciding when not to treat. The present review revisits the time‐honoured therapies available for HCM, in a practical perspective reflecting real‐world scenarios. Specific agents are presented with doses, titration strategies, pros and cons. Peculiar HCM dilemmas such as treatment of dynamic outflow obstruction, heart failure caused by end‐stage progression and prevention of atrial fibrillation and ventricular arrhythmias are assessed. In the near future, the field of HCM drug therapy will rapidly expand, based on ongoing efforts. Approaches such as myocardial metabolic modulation, late sodium current inhibition and allosteric myosin inhibition have moved from pre‐clinical to clinical research, and reflect a surge of scientific as well as economic interest by academia and industry alike. These exciting developments, and their implications for future research, are discussed.