Summary

[Posted 7/Nov/2022]

AUDIENCE: Cardiology, Oncology

KEY FINDINGS: LQRSVs are common but not ubiquitous in CA; they are more frequent in AL-CA than in ATTR-CA. LQRSVs reflect an advanced disease stage and independently predict CV death. In ATTR-CA, LQRSVs can provide incremental prognostic accuracy over the NAC staging system in patients with intermediate risk.

BACKGROUND: Low QRS voltages (LQRSVs) are a common electrocardiographic feature in patients with light chain amyloidosis (AL) and transthyretin amyloidosis (ATTR) cardiac amyloidosis (CA). The aim of this study was to identify clinical and echocardiographic correlates of LQRSV and to investigate their prognostic significance in patients with CA.

DETAILS: This was a multicenter, retrospective study performed in 6 CA referral centers including consecutive patients with AL- and ATTR-CA. LQRSVs were defined as a QRS amplitude <=5 mm (0.5 mV) in all peripheral leads. The study outcome was cardiovascular (CV) mortality. Overall, 411 (AL-CA: n = 120, ATTR-CA: n = 291) patients were included. LQRSVs were present in 66 (55%) patients with AL-CA and 103 (35%) with ATTR-CA (P < 0.001). In AL-CA, LQRSVs were independently associated with younger age (P = 0.015), higher New York Heart Association functional class (P = 0.016), and natriuretic peptides (P = 0.041); in ATTR-CA, LQRSVs were independently associated with pericardial effusion (P = 0.008) and lower tricuspid annulus peak systolic excursion (P = 0.038). During a median follow-up of 33 months (Q1-Q3: 21-46), LQRSVs independently predicted CV death in both AL-CA (HR: 1.76; 95% CI: 2.41-10.18; P = 0.031) and ATTR-CA (HR: 2.64; 95% CI: 1.82-20.17; P = 0.005). Together with the National Amyloidosis Centre (NAC) staging, LQRSVs provided incremental prognostic value in ATTR-CA (AUC for NAC model: 0.83 [95% CI: 0.77-0.89]; AUC for NAC + LQRSV model: 0.87 [95% CI: 0.81-0.93]; P = 0.040).

Copyright © American College of Cardiology Foundation. All rights reserved.

Source: Cipriani, A., De Michieli, L., Porari, A., et al. (2022). Low QRS Voltages in Cardiac Amyloidosis: Clinical Correlates and Prognostic Value. J Am Coll Cardiol CardioOnc.. Published: October 7, 2022. DOI: 10.1016/j.jaccao.2022.08.007.

Summary

[Posted 27/May/2026]

AUDIENCE: Infectious Disease, Family Medicine

KEY FINDINGS: A primary challenge in this specific outbreak is the nature of the causative agent, the Bundibugyo virus. Unlike the more common Zaire ebolavirus, there is currently no licensed vaccine or specific, FDA-approved treatment effective against the Bundibugyo strain. Consequently, the public health response relies entirely on traditional containment strategies. These include rapid case detection, patient isolation, meticulous contact tracing, the promotion of infection prevention and control practices, safe burial procedures, and robust community education to curb transmission chains. Researchers are currently evaluating whether existing therapeutic candidates or vaccine platforms could be adapted for emergency use, though clinical implementation remains under investigation.

BACKGROUND: In response to a burgeoning outbreak of Ebola virus disease caused by the Bundibugyo strain, the United States government has enacted new travel and entry protocols. The current outbreak, centered in the Democratic Republic of the Congo (DRC) and involving cases in South Sudan and Uganda, has prompted international health authorities to declare a public health emergency. As global travel remains a potential vector for the international spread of the virus, the U.S. government has taken proactive measures to bolster domestic defense against the introduction of the pathogen.

DETAILS: Effective May 2026, the U.S. Centers for Disease Control and Prevention (CDC) and the Department of Homeland Security have implemented stringent travel requirements. Foreign nationals who have visited the DRC, South Sudan, or Uganda within the 21 days prior to their arrival are temporarily suspended from entry into the United States. Furthermore, all U.S. citizens, nationals, and lawful permanent residents returning from these three countries must route their travel through specifically designated entry points, including Washington-Dulles International Airport, where they are subject to enhanced public health screening. These measures include health questionnaires, temperature checks using non-contact technology, and verification of contact information to facilitate monitoring for symptoms over a 21-day period following departure from the affected regions. While the current outbreak is significant—with reports indicating nearly 500 suspected cases and more than 130 deaths since the official declaration on May 15—the domestic risk to the United States is currently assessed by the CDC as low. As of late May 2026, no suspected, probable, or confirmed cases of Ebola have been reported within the United States. Authorities are maintaining a state of high readiness, with regional hospitals and state health departments prepared to manage and isolate any potential symptomatic travelers identified through the screening process.

Source: Centers for Disease Control and Prevention (CDC). Enhanced Ebola Airport Screening Begins at Washington-Dulles International Airport. U.S. Department of Health and Human Services. CDC. Published: May, 2026.

Summary

[Posted 25/May/2026]

AUDIENCE: Cardiology, Endocrinology, Internal Medicine

KEY FINDINGS: Sam68 is a stress-activated cardiomyocyte scaffold that drives pathologic hypertrophy through a Src-STAT3-PDK4 program that inhibits PDH and suppresses glucose oxidation. Genetic or pharmacologic disruption of this axis restores PDH-dependent pyruvate oxidation and limits pressure-overload remodeling, identifying Sam68 as a druggable metabolic control node in heart failure.

BACKGROUND: Metabolic remodeling, marked by maladaptive shifts in substrate use and energy production, is a hallmark of pathologic cardiac hypertrophy. Yet the mechanisms linking stress signaling to impaired myocardial glucose oxidation remain incompletely defined. Sam68 (Src-associated in mitosis, 68 kDa; also known as KHDRBS1 [KH domain-containing, RNA-binding, signal transduction-associated protein 1]), a STAR (signal transduction and activation of RNA) family RNA-binding protein, has not previously been implicated in cardiac metabolic control.

DETAILS: Sam68 expression was examined in failing human hearts and transcriptomic data sets. Cardiomyocyte-specific Sam68 knockout mice (Sam68cKO) and AAV9 (adeno-associated virus serotype 9)-cTnT (cardiac troponin T)-mediated cardiomyocyte Sam68 overexpression (Sam68OE) were studied in transverse aortic constriction and angiotensin II models. Mechanistic studies included RNA sequencing, targeted metabolomics, in vivo [U-¹³C]-glucose tracing, coimmunoprecipitation, and protein-protein docking. Therapeutic relevance was tested with a PDK4 (pyruvate dehydrogenase kinase 4) inhibitor and the Sam68-Src interface blocker YB-0158, including pharmacokinetics, target engagement, and validation in Sam68cKO mice. Sam68 was increased in failing human cardiomyocytes and in murine hypertrophic hearts. Sam68cKO markedly attenuated angiotensin II- and transverse aortic constriction-induced hypertrophy, whereas Sam68OE aggravated remodeling and dysfunction. In vivo [U-¹³C]-glucose flux analysis showed that transverse aortic constriction caused sustained uncoupling of glycolysis from glucose oxidation, with increased glycolytic labeling but reduced ¹³C incorporation into tricarboxylic acid cycle intermediates at 3 days and 4 weeks. Sam68 deletion restored glucose-derived carbon entry into the tricarboxylic acid cycle, enhanced PDH (pyruvate dehydrogenase)-dependent M+2 labeling, and improved oxidative-anaplerotic balance during pressure overload. Mechanistically, Sam68 served as a stress-activated scaffold that promoted Src-dependent STAT3 (signal transducer and activator of transcription 3) Tyr705 phosphorylation, nuclear accumulation, and transcriptional induction of PDK4, leading to PDH Ser293 phosphorylation and suppression of PDH activity. The PDK4 inhibitor blunted Sam68OE-driven remodeling while preserving PDH activity and mitochondrial respiratory programs. YB-0158 achieved cardiac exposure, disrupted Sam68-Src engagement in vivo, suppressed STAT3-PDK4-PDH signaling, and improved transverse aortic constriction remodeling; these effects were lost in Sam68cKO mice, supporting on-target dependence. In failing human hearts, the Src-Sam68-STAT3-PDK4 axis was activated, and Sam68 abundance increased in parallel with PDK4 and reduced left ventricular ejection fraction.

Copyright © American Heart Association, Inc. All rights reserved.

Source: An, J., Han, C., Jiang, Y., et al. Sam68 Exacerbates Pathologic Cardiac Hypertrophy by Suppressing Cardiomyocyte Glucose Oxidation. Circulation. Published: May, 2026. DOI: 10.1161/CIRCULATIONAHA.125.07753

Summary

A Randomized Controlled Comparative Study

[Posted 19/May/2026]

AUDIENCE: General Surgery, Family Medicine

KEY FINDINGS: Early active treatment with isotretinoin and FMRF is safe and better than isotretinoin monotherapy over 44 weeks regarding severity, reduced erythema, and improved surface roughness in moderate-to-severe acne vulgaris. This encourages early and effective treatment of acne to mitigate acne scarring and improve patients' quality of life.

BACKGROUND: Oral isotretinoin is the standard therapy for severe acne. However, scarring may persist. Fractional microneedling radiofrequency (FMRF) improves both inflammatory lesions and scars with minimal downtime. In this study, we compare isotretinoin monotherapy and concurrent isotretinoin and FMRF for active acne regarding clinical outcomes. The GAGS scores of isotretinoin and FMRF were significantly lower than those of isotretinoin monotherapy from weeks 12-44 (-79.69% vs. -60.34% at week 44, respectively; p < 0.001). Isotretinoin and FMRF showed significantly greater lesion count reductions than isotretinoin monotherapy at follow-up visits from weeks 12-44. Isotretinoin and FMRF showed significantly lower hemoglobin levels than isotretinoin monotherapy at weeks 32 and 44 (p = 0.029 and p < 0.001, respectively). Skin surface roughness improved substantially and persistently from week 12-44.

DETAILS: In this parallel two-group comparative study, patients received either low-dose isotretinoin monotherapy for 20 weeks (n = 34) or low-dose isotretinoin concurrently with 5 monthly FMRF sessions (n = 36). Outcomes were assessed at baseline and weeks 12, 20, 24, 32, and 44. The primary endpoints were Global Acne Grading System (GAGS) scores and inflammatory/non-inflammatory lesion counts. Secondary endpoints were hemoglobin indices and skin roughness.

Copyright © Wiley Periodicals LLC. All rights reserved

Source: Disphanurat, W., Leeyangyuen, P,, and Srisantithum, B. Efficacy of Low-Dose Oral Isotretinoin Combined With Fractional Microneedle Radiofrequency Versus Low-Dose Oral Isotretinoin Monotherapy in the Treatment of Moderate-To-Severe Acne Vulgaris: A Randomized Controlled Comparative Study. Lasers in Surgery and Medicine. 2026; 58(4): 321-330. Published: April, 2026. DOI: 10.1002/lsm.70120.

Summary

[Posted 11/May/2026]

AUDIENCE: All Healthcare Professionals

KEY FINDINGS:

• Hantaviruses are a family of viruses that cause serious illness and sometimes death in people worldwide.
• The viruses are spread by infected rodents through their urine, feces, and saliva.
• Some hantaviruses cause hantavirus pulmonary syndrome (HPS).
• Early symptoms of HPS in people resemble many other respiratory illnesses, making HPS difficult to diagnose at illness onset.
• Healthcare providers should test a person for hantavirus if they have HPS-compatible symptoms and have had contact with rodents.

BACKGROUND: Hantaviruses are spread by rodents' body fluids and excrement. People mostly contract hantavirus by breathing in the virus. Most hantaviruses found in North, Central, and South America can cause hantavirus pulmonary syndrome (HPS). Andes virus, which is found in South America, has reportedly had person-to-person transmission.

DETAILS: Different hantaviruses are found in the United States. Most of these cause HPS, which primarily affects the lungs. Non-HPS hantavirus infection can also occur, where patients experience non-specific viral symptoms, but no cardiopulmonary symptoms. The hantaviruses that are found throughout the United States are not known to spread between people.

HPS initially causes flu-like symptoms that can progress to more severe illness where people have trouble breathing. It's important for people with HPS to begin treatment as early as possible to improve their chances of recovery. HPS is fatal in nearly 4 in 10 people who are infected.

Exposure risks

Anyone who has contact with hantavirus-carrying rodents, or their droppings, urine, saliva or nesting material is at risk of HPS. Rodent infestation in and around the home remains the primary risk for hantavirus exposure. Even healthy individuals are at risk for HPS infection if they have contact with the virus.

Andes virus can cause HPS and is the only type of hantavirus that is known to spread person-to-person.

How it spreads

Each hantavirus has one primary rodent that carries the disease. The most common hantavirus that causes HPS in the U.S. is spread by the deer mouse.

People can contract hantavirus if they have contact with urine, feces or saliva of a rodent carrying the virus. This can occur when people:

1. Breathe in hantavirus-contaminated air when cleaning up after rodents.
2. Touch contaminated objects and then touch their nose or mouth.
3. Are bitten or scratched by an infected rodent.
4. Eat food contaminated with hantavirus.

Cases normally occur in rural areas where forests, fields, and farms offer habitats for rodents. The animals can get into homes and barns, where they may leave urine or feces.

Dogs and cats are not known to become infected with hantavirus in the United States. Pets may bring infected rodents to people or into homes.

Testing and diagnosis

Assessing patients for hantavirus can be difficult early in the infection because symptoms are non-specific and resemble many other viral infections like influenza, legionnaire's, leptospirosis, mycoplasma, and Q fever. Because hantavirus resembles these infections, a blood test is often the only way to officially diagnose it.

To diagnose hantavirus or HPS, clinicians should understand:

• Disease symptoms and rodent exposure history
• Testing guidelines to identify the virus
• How to request testing support from CDC if needed, and
• How to report cases to CDC

Clinicians with a patient experiencing symptoms compatible with HPS and a potential rodent exposure should contact their state, tribal, local, or territorial health department.

Testing

CDC uses an enzyme-linked immunosorbent assay (ELISA) to detect IgM antibodies and diagnose acute infections with hantaviruses. This diagnostic method is used to diagnose both HPS and HFRS. Diagnostic testing can be performed at:

1. CDC
2. State labs running the CDC-developed assay
3. State public health labs using other diagnostic assays
4. Commercial labs

The criteria to report hantavirus-positive cases are based on the national case definition, which includes clinical symptoms (HPS or non-HPS) and acute laboratory diagnostic results, such as:

1. IgM positive
2. IgG positive with rising titers
3. Immunohistochemistry positive, or
4. PCR positive

Treatment and recovery

There is no specific treatment for hantavirus infection. If HPS is suspected, the patient needs emergency medical care immediately, preferably in the intensive care unit, even before diagnosis.

Early intensive medical care is critical because patients who have sudden acute disease can rapidly become severely sick and die. If a patient is experiencing full distress, it is less likely the treatment will be effective.

Patient management should include:

1. Monitoring and adjustment of cardiac function
2. Carefully administering fluids
3. Providing supplemental oxygen
4. Intubating and ventilating if needed

Suspected HPS patients should receive appropriate broad-spectrum antibiotic therapy, even if you're still waiting for diagnosis. Care should also include fever reducers and pain relievers.

While HPS can be quite severe, it has a short duration of critical disease. The cardiopulmonary dysfunction seen in HPS is most likely due to circulating inflammatory mediators. Autopsies performed on fatal cases did not show significant tissue damage.

Initiating extracorporeal membrane oxygenation (ECMO) at the earliest sign of decompensation has an 80 percent survival rate in patients despite cardiopulmonary collapse.

Within 24 hours of initial evaluation, most HPS patients develop some degree of hypotension. They also experience progressive evidence of pulmonary edema and hypoxia, usually requiring mechanical ventilation.

Patients with fatal infections often appear to have severe myocardial depression that progresses to sinus bradycardia with subsequent electromechanical dissociation, ventricular tachycardia, or fibrillation.

In patients with HPS, poor prognostic indicators include a plasma lactate of greater than 4.0 mmol/L or a cardiac index of less than 2.2 L/min/m2.

Pulmonary edema and pleural effusions are common, but multiorgan dysfunction syndrome is rarely seen. However, HPS patients sometimes have mildly impaired renal function. Survivors frequently become polyuric during convalescence and improve rapidly.

Intravenous ribavirin, a guanosine analogue, has been tested in patients with HPS. However, it was not shown to be effective for treatment of HPS.

Without adequate treatment, most deaths occur in patients with HPS within 24 to 48 hours of the cardiopulmonary phase onset.

Related diseases

Some hantaviruses cause kidney symptoms more than lung damage. When this occurs, it is called hemorrhagic fever with renal syndrome (HFRS).

Source: Clinician Brief: Hantavirus Pulmonary Syndrome (HPS). CDC. Published: May 8, 2026.

Summary

[Posted 8/May/2026]

AUDIENCE: Infectious Disease, Family Medicine

KEY FINDINGS: In two open-label trials, nirmatrelvir-ritonavir did not reduce the incidence of hospitalization or death among vaccinated higher-risk participants with SARS-CoV-2 infection.

BACKGROUND: Nirmatrelvir-ritonavir has been shown to reduce progression to severe illness from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in unvaccinated high-risk outpatients. The effectiveness of nirmatrelvir-ritonavir in persons who have been vaccinated, infected naturally, or both is unclear.

DETAILS: In two open-label platform trials (PANORAMIC in the United Kingdom and CanTreatCOVID in Canada), we enrolled higher-risk adults (>=50 years of age or >=18 years of age with coexisting conditions) in the community who tested positive for SARS-CoV-2 and had been unwell for 5 days or less. The participants were randomly assigned to receive usual care plus nirmatrelvir (300 mg)-ritonavir (100 mg) twice a day for 5 days or to receive usual care alone. The primary outcome was hospitalization or death from any cause within 28 days after randomization. From December 8, 2021, to September 30, 2024, a total of 3516 participants in the PANORAMIC trial and 716 participants in the CanTreatCOVID trial underwent randomization. In the PANORAMIC trial, 14 of 1698 participants (0.8%) in the nirmatrelvir-ritonavir group and 11 of 1673 participants (0.7%) in the usual-care group were hospitalized or died (adjusted odds ratio, 1.18; 95% Bayesian credible interval, 0.55 to 2.62; probability of superiority, 0.334). In the CanTreatCOVID trial, 2 of 343 participants (0.6%) in the nirmatrelvir-ritonavir group and 4 of 324 participants (1.2%) in the usual-care group were hospitalized or died (adjusted odds ratio, 0.48; 95% Bayesian credible interval, 0.08 to 2.23; probability of superiority, 0.830). In a substudy involving 634 participants, viral load was reduced by the end of treatment with nirmatrelvir-ritonavir. Serious adverse events with nirmatrelvir-ritonavir were reported in 9 participants in the PANORAMIC trial and in 4 participants in the CanTreatCOVID trial.

Copyright © Massachusetts Medical Society. All rights reserved.

Source: Butler, C. C., Pinto, A. D., Harris, V., et al. Oral Nirmatrelvir-Ritonavir for Covid-19 in Higher-Risk Outpatients. N Engl J Med. 2026; 394(16): 1583-1594. Published: April 22, 2026. DOI: 10.1056/NEJMoa2502457