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Treatment for heart failure has experienced a major revolution in recent years, and current evidence shows that a combination of four medications (angiotensin receptor-neprilysin inhibitors + ß-blockers + mineralocorticoid receptor antagonists + sodium.glucose cotransporter 2 inhibitors) offer the greatest benefit to our patients with significant reductions in cardiovascular mortality, heart failure hospitalisations and all-cause mortality. Unfortunately, despite their proven benefits, the implementation of these therapies is still low. Clinical inertia, and unfounded fear of using these drugs might contribute to this. Recently, evidence from randomised clinical trials has shown that intensive implementation of these therapies in patients with heart failure is safe and effective. In this review, we attempt to tackle some of these misconceptions/fears regarding medical therapy for heart failure and discuss the available evidence showing the best strategies for implementation of these therapies.

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Atorvastatin is widely recommended for long-term secondary prevention in STEMI patients with no contraindication. Although high-dose atorvastatin has been shown to reduce important patient outcomes such as MACE, there is still doubt that high-dose atorvastatin could have the same protective effect in patients undergoing PCI in the short and long term. We searched the following electronic databases: Scopus, Web of Science, MEDLINE, EMBASE, and Cochrane Central considering studies that enrolled adult patients with a confirmed diagnosis of STEMI or NSTEMI undergoing PCI. The intervention must have been atorvastatin alone compared to a placebo, standard care, or a different atorvastatin dose. A total of (n = 11) studies were included in the quantitative analysis. Information on (N = 5,399) patients was available; 2,654 were assigned to receive high-dose atorvastatin therapy, and 2,745 comprised the control group. High-dose atorvastatin pre-loading significantly reduced MACE at one month of follow-up (RR: 0.78; 95% CI: 0.67-0.91; p = 0.014) in both STEMI and NSTEMI. All-cause mortality was reduced in patients with STEMI (RR: 0.28; 95% CI: 0.10-0.81; p = 0.029). The quality of the body of evidence was rated overall as moderate. Patients presenting with STEMI or NSTEMI benefit from high-dose atorvastatin pre-loading before PCI by reducing MACE at 30 days. The use of high-dose atorvastatin in STEMI patients reduced all-cause mortality. The beneficial effects of atorvastatin pre-loading are limited to 30 days post-PCI.

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BACKGROUND: Cardiovascular manifestations in patients with COVID-19 are associated with dire outcomes. Long COVID syndrome is the persistence of symptoms after acute disease and is found in up to 40% of subjects. There is little information regarding subacute echocardiographic manifestations after COVID-19, and no study has included a Mexican mestizo population. METHODS: This cross-sectional study included subjects older than 18 with an episode of COVID-19 in the last 3 months. Those with previously known cardiovascular disease were excluded. The patient´s medical history and COVID-19 information were obtained from clinical charts. We performed a transthoracic echocardiogram in every subject and determined left ventricular (LV) index mass, LV ejection fraction (LVEF), left ventricular global longitudinal strain (LV GLS), right ventricular (RV) GLS, and tricuspid annular plane systolic excursion (TAPSE). A descriptive and comparative analysis was performed based on symptom severity and persistence. RESULTS: One hundred subjects were included; 63% were classified with mild and 37% with moderate to severe COVID-19. The median of LVEF was 60% (55-60), LV GLS and RV GLS was impaired in 34% and 74% of patients, respectively. Patients with moderate to severe disease had significantly lower LVEF (Mean Difference: -3.3), TAPSE (mean difference: -1.8), and higher (worse) LV GLS (Mean Difference: 2.5) and RV GLS (mean difference: 2.9). Persistent symptoms were associated with lower TAPSE and higher RVGLS. CONCLUSIONS: Patients who recover from COVID-19 have a high prevalence of subtle RV and LV dysfunction using GLS analysis. A moderate to severe episode was associated with worse RV and LV function measured by RV GLS, TAPSE, and LV GLS. Subjects with persistent symptoms had worse RVGLS and TAPSE.

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In accidental intoxicated animals and humans, Karwinskia humboldtiana (Kh) causes lesions in the central and peripheral nervous system and organs like the kidney, liver, and lung. The objective was to evaluate the histology of myocardium and skeletal muscle after experimental chronic intoxication with mature fruit of Kh in Wistar rat. Twenty-five rats were used and divided into five groups (n = 5): four intoxicated and one control. Kh fruit was ground, dried, sieved, and administered by an orogastric tube. Intoxicated rats received 3.5 g/kg body weight fractionated in 5 doses. Control rats received only water. Animals were euthanized at 24, 48, 58, and 112 days, respectively. Samples of the myocardium and skeletal muscle were obtained and processed for light microscopy evaluation. Morphological analyses were performed, including a microdensitometric analysis. Results showed areas of necrosis in the muscle fibers, fibers with vacuolated cytoplasm, and disorganization of myofilaments, as well as staining variations in both myocardium and skeletal muscle time-depending. Zones with loss of continuity of the external lamina were identified with PAS with the diastase histochemical method. Immunolabeling with specific antibodies demonstrated diminution of actin and desmin myofilaments. The microdensitometric analysis showed a statistically significant difference between the intoxicated vs control group. These findings demonstrate that chronic intoxication of Kh fruit also causes damage in myocardial and skeletal muscle, these alterations will be useful to understand that the toxic effects of Kh fruit in accidently intoxicated humans are systemic, and not only over the nervous system.

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Round pneumonia is an unusual radiological manifestation of a bacterial lung infection. We present the case of an elderly male patient who arrived at the emergency room with a productive cough and exertional dyspnea. His chest x-ray and CT showed a round opacity and air bronchograms in the right upper lobe. Taken together, the patient's symptoms and images strongly suggest a pulmonary infection. Empirical antibiotic therapy with ceftriaxone and clarithromycin was started. The sputum culture was positive for Enterobacter hormaechei and the bacterium was sensitive to levofloxacin; therefore, the antibiotic therapy was changed. Despite the treatment, the patient progressed to respiratory failure and septic shock, dying six days after admission. Although round pneumonia is uncommon, it is a potentially curable disease and clinicians should always consider it in their differential diagnosis.

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Coccidioidomycosis is an endemic disease of arid regions in the Western hemisphere. Its clinical presentation varies from asymptomatic nodules on chest x-rays to disseminated disease. We present the case of a 48-year-old man with a hard and heterogeneous tumor in the posterior aspect of the right testis. Color flow doppler testicular ultrasonography was performed and two nodular masses in the tail of the right epididymis were identified. An epididymectomy was performed and histopathological examination revealed coccidioidomycosis. After diagnosis, the patient was successfully treated with fluconazol.

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A 48-year-old male with a prior diagnosis of diabetes mellitus presented to the emergency department with malaise and nausea. On work-up, he was found with hyperglycemia and high anion gap metabolic acidosis, with a blood pH < 6.94. A diagnosis of severe diabetic ketoacidosis was established; serum electrolyte analysis showed mild hyperkalemia. On work-up, a 12-lead electrocardiogram was obtained, and it showed an ST-segment elevation on anterior leads that completely resolved with diabetic ketoacidosis treatment. ST-segment elevation myocardial infarction can be a precipitant factor for diabetic ketoacidosis, and evaluation of diabetic patients with suspected myocardial infarction can be challenging since they can present with atypical or little symptoms. Hyperkalemia, which usually accompanies diabetic ketoacidosis, can cause electrocardiographic alterations that are well described, but ST-segment elevation is uncommon. A pseudomyocardial infarction pattern has been described in patients with diabetic ketoacidosis; of note, most of these patients presented severe hyperkalemia. We believe this is of great importance for clinicians because they must be able to recognize those patients that present with electrocardiographic abnormalities secondary to the metabolic alterations and those that can be experiencing actual ongoing ischemia, in order to establish an appropriate and prompt treatment.

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