Rethinking clinical decision-making to improve clinical reasoning

: Improving clinical reasoning techniques is the right way to facilitate decision-making from prognostic, diagnostic, and therapeutic points of view. However, the process to do that is to fill knowledge gaps by studying and growing experience and knowing some cognitive aspects to raise the awareness of thinking mechanisms to avoid cognitive errors through correct educational training. This article examines clinical approaches and educational gaps in training medical students and young doctors. The authors explore the core elements of clinical reasoning, including metacognition, reasoning errors and cognitive biases, reasoning strategies, and ways to improve decision-making. The article addresses the dual-process theory of thought and the new Default Mode Network (DMN) theory. The reader may consider the article a first-level guide to deepen how to think and not what to think, knowing that this synthesis results from years of study and reasoning in clinical practice and educational settings

A hidden echocardiographic pitfall: the Gerbode defect

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Hypoadiponectinemia: A Link between Visceral Obesity and Metabolic Syndrome

Metabolic syndrome (MetS) represents a combination of cardiometabolic risk factors, including visceral obesity, glucose intolerance or type 2 diabetes, elevated triglycerides, reduced HDL cholesterol, and hypertension. MetS is rapidly increasing in prevalence worldwide as a consequence of the “epidemic” obesity, with a considerable impact on the global incidence of cardiovascular disease and type 2 diabetes. At present, there is a growing interest on the role of visceral fat accumulation in the occurrence of MetS. In this review, the effects of adipocytokines and other proinflammatory factors produced by fat accumulation on the occurrence of the MetS have been also emphasized. Accordingly, the “hypoadiponectinemia” has been proposed as the most interesting new hypothesis to explain the pathophysiology of MetS

Optimized search strategy for detecting scientifically strong studies on treatment through PubMed

Our study was designed to optimize the search strategies based on the work of Haynes et al. for detecting randomized controlled trials (RCTs) through PubMed. In particular, we aimed to improve precision for broad and narrow searches on interventional studies. We used in addition to the string suggested by the Hedge Team the following: {NOT ((animals [mh] NOT humans [mh]) OR (review [pt] OR meta-analysis [pt]))} and tested its effectiveness. The search was carried out on a year's worth of articles from the PubMed database. We analyzed 35,590 bibliographic citations about four relevant major topics in internal medicine (hypertension, diabetes, heart failure, and hepatitis). Precision, percentage gain between the Hedge Team search strategies and the new one were computed and reported in the text. Moreover, a pooled analysis was carried out in terms of absolute precision difference. We observed better precision for both broad and narrow searches. However, effective gain resulted only for broad searches. In this case, bibliographic citation recall effectively reduced (-24 to -35 % retrieved citation with a gain of 32-54 %) without loss of information. The search strategy improved broad searches regarding each of the four considered topics. We think this new search strategy, based on a previous work of the Hedge team, could be a step forward and can save some time by researchers

Plasma adiponectin: A contributing factor for cardiac changes in visceral obesity-associated hypertension

This study has been designed to evaluate the impact of adiponectin levels on left ventricular geometry and function in visceral obesity-associated hypertension. 94 consecutive subjects, 53 of them were hypertensives and 41 normotensives with age <= 65 years, subgrouped according to the presence or absence of visceral obesity, were studied. Total adiponectin levels were measured by a validated competitive radioimmunoassay. Left ventricular telediastolic internal diameter, interventricular septum, posterior wall thickness, total left ventricular mass (LVM) and normalized for height to the 2.7 power (LVM/h(2.7)), relative wall thickness, left ventricular ejection fraction by echocardiography and isovolumic relaxation time, E/A ratio and deceleration time of E velocity, by pulsed-wave Doppler, were calculated. Plasma adiponectin levels were significantly lower in visceral obesity-associated hypertensives than lean hypertensives (p < 0.001) and in lean normotensives (p < 0.001). LVM and LVM/h(2.7) were significantly (p < 0.05) higher in both hypertensive groups, and in visceral obesity-associated normotensives in comparison with lean normotensives. Adiponectin levels correlated inversely with LVM/h(2.7) but only in normotensives (adjusted R squared 0.77, p < 0.0001) and hypertensives (0.67, p < 0.0001) subjects with visceral obesity. Multiple regression analysis indicated that adiponectin levels remain significantly associated (p < 0.001) to LVM/h(2.7) also when adjusted for age, gender, body mass index, waist to hip ratio and mean blood pressure. Our data suggest an important role of adiponectin in increased LVM/h(2.7) in visceral obesity-associated normotensive and hypertensive subjects. In this last group, adiponectin, more than blood pressure, may be able to explain the development of cardiac damage.This study has been designed to evaluate the impact of adiponectin levels on left ventricular geometry and function in visceral obesity-associated hypertension. 94 consecutive subjects, 53 of them were hypertensives and 41 normotensives with age ≤ 65 years, subgrouped according to the presence or absence of visceral obesity, were studied. Total adiponectin levels were measured by a validated competitive radioimmunoassay. Left ventricular telediastolic internal diameter, interventricular septum, posterior wall thickness, total left ventricular mass (LVM) and normalized for height to the 2.7 power (LVM/h2.7), relative wall thickness, left ventricular ejection fraction by echocardiography and isovolumic relaxation time, E/A ratio and deceleration time of E velocity, by pulsed-wave Doppler, were calculated. Plasma adiponectin levels were significantly lower in visceral obesity-associated hypertensives than lean hypertensives (p < 0.001) and in lean normotensives (p < 0.001). LVM and LVM/h2.7 were significantly (p < 0.05) higher in both hypertensive groups, and in visceral obesity-associated normotensives in comparison with lean normotensives. Adiponectin levels correlated inversely with LVM/h2.7 but only in normotensives (adjusted R squared 0.77, p < 0.0001) and hypertensives (0.67, p < 0.0001) subjects with visceral obesity. Multiple regression analysis indicated that adiponectin levels remain significantly associated (p < 0.001) to LVM/h2.7 also when adjusted for age, gender, body mass index, waist to hip ratio and mean blood pressure. Our data suggest an important role of adiponectin in increased LVM/h2.7 in visceral obesity-associated normotensive and hypertensive subjects. In this last group, adiponectin, more than blood pressure, may be able to explain the development of cardiac damage

May Adiponectin be considered as a Novel Cardiometabolic Biomarker?

This study was designed to evaluate the interaction between total adiponectin (ADPN) and metabolic syndrome (MetS) on cardiac changes in 135 subjects with and without MetS, subgrouped according to normal or low ADPN. Left ventricular internal diameter (LVID/h), LV mass (LVM), LVM index (LVMI), interventricular septal thickness (IVST), relative wall thickness (RWT) and LV ejection fraction (EF) by echocardiography and diastolic parameters, by pulsed-wave Doppler were calculated. BMI, LVM, LVMI, LVID/h, IVST and RWT values were significantly (p<0.05) higher in both groups with low ADPN. Prevalence of left ventricular hypertrophy (p<0.001) and coronary artery disease (p<0.01) was significantly higher in both low ADPN groups. LVMI correlated directly with BMI (p<0.001), (p<0.001), MetS (p<0.001) and inversely with ADPN (p<0.0001). ADPN and BMI resulted independently associated with LVMI. In conclusion, our data suggest that hypoadiponectinemia might be considered a novel “cardiometabolic biomarker”. Accordingly, circulating ADPN might become a new target in the management of cardiometabolic syndrome

Antihypertensive and cardiovascular effects of combined blockade of renin-angiotensin system with ACE inhibitor and angiotensin II type 1 receptor blocker in hypertensive patients: A 24-week randomized controlled double-dummy trial

Background. In this study the effects of 24 weeks losartan and ramipril treatment, both alone and in combination, on blood pressure and left ventricular mass (LVM) and function, have been evaluated in hypertensives. Methods. 57 hypertensives with stage 1 and 2 essential hypertension were included. After 4 weeks run in, a randomized double-blind, 3 arm, double dummy, independent trial was used. All patients were randomly allocated to 3 treatment arms consisting of losartan (50 mg/daily), ramipril (5 mg/daily), and combined (losartan 50 mg/ramipril 5 mg/daily) for 24 weeks. LVM, LVM/h2.7 and other echocardiographic measurements, BUN, creatinine and clearance and potassium were determined after run in and 24 weeks. Results. All groups were comparable for gender, age, BMI, BP and LVM. The prevalence of baseline left ventricular hypertrophy (LVH) was not significantly different among 3 groups. At the end of treatment, a significant (p&lt;0.05) reduction in SBP, DBP, MBP, LVM and LVM/h2.7 were observed in all groups. The absolute and percent reduction in LVM/h2.7 were significantly higher in combined than losartan or ramipril groups and also in hypertensives with LVH. No significant change in absolute and percent reduction of SBP, DBP and MBP were found. Conclusions. These data indicate an additional cardioprotective effect of dual blockade of RAS in hypertensive patients with and without left ventricular hypertrophy