Despite the iconoclasts of the LDL-centric principle and the net benefit of statins, the plurality, quantity, and especially the scientific quality of the evidence that supports the causal role of low-density lipoprotein cholesterol (LDL-C) in atherosclerosis, as well as the net benefit of statins in its prevention, make these two concepts, universal principles accepted by all guidelines worldwide. The efficacy, safety, and cost-effectiveness of statins have been confirmed in multiple randomized and controlled clinical trials. However, paradoxically, and especially in developing countries like Mexico, the use of this therapeutic class is suboptimal. The reasons to explain this paradox are multiple and are analyzed in this article, which has the purpose of confirming the efficacy, safety, and significant potential impact of statins in the "real developing world." To fulfill this purpose, this article presents our center experience using statins, especially atorvastatin®, in patients without atherosclerotic cardiovascular disease (ASCVD). Founded on an evidence-based, personalization, and empowerment program, our results in almost four hundred patients in primary cardiovascular prevention are as follows. In intermediate-risk patients, atorvastatin® 10 mg/day with a baseline LDL-C of 111.6 mg/dL (±25.1), reduced LDL-C by 38.0% (±13.9); atorvastatin® 20 mg/day with a baseline LDL-C of 124.4 mg/dL (±25.3), reduced LDL-C by 44.9% (±15.0) (p <0.005 for both). In the atorvastatin® 10/20 mg/day cohort (a total of 294 patients), 87.7% (258 patients) achieved a ≥30% LDL-C reduction, and 36.7% (108 patients) a ≥50% reduction. In the atorvastatin 10/20 mg/day cohort, with an average baseline LDL-C of 122.6 mg/dL (±25.6), 92.5 and 55.7% achieved LDL-C of ≤100 and ≤70 mg/dL, respectively. In high-risk patients, atorvastatin® 40 mg/day with a baseline LDL-C of 151.7 mg/dL (±31.6), there was an LDL-C average reduction of 54.7% (±12.2). Atorvastatin 80mg/day with a baseline LDL-C of 160.2 mg/dL (±41.5) produced an LDL-C average reduction of 62.5% (±10.8) (P <0.005 for both). In the atorvastatin® 40/80 mg/day cohort (89 patients), 98.8% (88 patients) achieved a ≥30% LDL-C reduction, and 76.4% (68 patients) achieved a ≥50% reduction. In the atorvastatin 40/80 mg/day cohort, with an average baseline LDL-C of 153.0 mg/dL (±33.2), 95.8 and 62.9% achieved LDL-C of ≤100 and ≤70 mg/dL, respectively.

In patients with hypertension (HT), cardiovascular risk reduction is directly proportional to the reduction in blood pressure sustained over time. However, in “real life,” blood pressure control is often insufficient or not sustained over time to achieve optimal cardiovascular risk reduction. In this article, we comment on the multiple reasons which explain this common therapeutic failure. Also, in this article, we summarize the amazing basic and clinical phase III evidence of azilsartan (AZL) and azilsartan combined with chlortalidone (CLD), two excellent therapeutic options for HT control. With such evidence as scientific background, we communicate our results with almost 300 HT patients treated with azilsartan and azilsartan/chlortalidone in "real life." In brief, our findings were the following: a) In HT patients with blood pressure (BP) <150/90 mmHg, AZL 40 mg as monotherapy provides practically 100% success to achieve a target BP <140/90 and <130/80 mmHg, in a subpopulation that we have called “hyper-responders” b) In HT patients with BP <150/90 mmHg (naive or with another treatment failure), AZL/CLD 40/12.5 mg provides practically 100% success to achieve a target BP <140/90 mmHg and 90% to achieve a target BP <130/80 mmHg; c) In HT patients with BP >150/90 mmHg (generally with another treatment failure), AZL/CLD 80/12.5 mg gives women a success rate greater than 60% to achieve a target BP <140/90 mmHg and greater than 50% to achieve a target BP <130/80 mmHg. The success rates were higher in men, greater than 75% to achieve a target BP <140/90 mmHg and greater than 60% to achieve a target BP <130/80 mmHg. In both cases, the use of amlodipine (2.5, 5, or 10 mg) made it possible to achieve a target BP <140/90 mmHg in 100% of the cases and <130/80 mmHg in 80% of the cases. Finally, according to our results, we propose a simple three-step strategy based on evidence, personalization, and empowerment which allows reaching a target BP <140/90 mmHg in more than 90% of cases and a target BP <130/80 mmHg in more than 75% of cases in 4 to 12 weeks.

Manipulating the action of the Cholesteryl Ester Transfer Protein-CETP-and transforming the human lipid phenotype into one resembling the mouse lipid phenotype, in order to reduce susceptibility to atherosclerosis, is a hypothesis based on at least three lines of scientific evidence summarized within the introduction of this article. The following aspects related to the pharmacological manipulation of the CETP are discussed within the present article: a) CETP as a controversial protein involved in heterotypic and homotypic transport of neutral lipids between different lipoproteins; b) CETP as a protein involved in atherogenic dyslipidemia associated with the insulin resistance syndrome and c) pharmacological manipulation of the CETP by using "second generation" drugs-dalcetrapib, anacetrapib and evacetrapib-focusing on the results of Phase IIb and Phase III studies published up to May 2012. The article concludes with a review of the strengths, weaknesses, opportunities and current controversy on the HDL-centric versus LDL-centric theories.