Sex and Racial Disparities in Proportionate Mortality of Premature Myocardial Infarction in the United States: 1999 to 2020.

BACKGROUND: The incidence of premature myocardial infarction (PMI) in women (<65 years and men <55 years) is increasing. We investigated proportionate mortality trends in PMI stratified by sex, race, and ethnicity. METHODS AND RESULTS: CDC WONDER (Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research) was queried to identify PMI deaths within the United States between 1999 and 2020, and trends in proportionate mortality of PMI were calculated using the Joinpoint regression analysis. We identified 3 017 826 acute myocardial infarction deaths, with 373 317 PMI deaths corresponding to proportionate mortality of 12.5% (men 12%, women 14%). On trend analysis, proportionate mortality of PMI increased from 10.5% in 1999 to 13.2% in 2020 (average annual percent change of 1.0 [0.8-1.2, P <0.01]) with a significant increase in women from 10% in 1999 to 17% in 2020 (average annual percent change of 2.4 [1.8-3.0, P <0.01]) and no significant change in men, 11% in 1999 to 10% in 2020 (average annual percent change of -0.2 [-0.7 to 0.3, P=0.4]). There was a significant increase in proportionate mortality in both Black and White populations, with no difference among American Indian/Alaska Native, Asian/Pacific Islander, or Hispanic people. American Indian/Alaska Natives had the highest PMI mortality with no significant change over time. CONCLUSIONS: Over the last 2 decades, there has been a significant increase in the proportionate mortality of PMI in women and the Black population, with persistently high PMI in American Indian/Alaska Natives, despite an overall downtrend in acute myocardial infarction-related mortality. Further research to determine the underlying cause of these differences in PMI mortality is required to improve the outcomes after acute myocardial infarction in these populations.

Coronavirus disease 2019 (COVID-19): Multisystem review of pathophysiology.

Coronavirus disease-19 (COVID-19) pandemic is associated with high morbidity and mortality. COVID-19, which is caused by the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS CoV-2), affects multiple organ systems through a myriad of mechanisms. Afflicted patients present with a vast constellation of symptoms, from asymptomatic disease to life-threatening complications. The most common manifestations pertain to mild pulmonary symptoms, which can progress to respiratory distress syndrome and venous thromboembolism. However, in patients with renal failure, life-threatening cardiac abnormalities can ensue. Various mechanisms such as viral entry through Angiotensin receptor (ACE) affecting multiple organs and thus releasing pro-inflammatory markers have been postulated. Nevertheless, the predictors of various presentations in the affected population remain elusive. An ameliorated understanding of the pathology and pathogenesis of the viral infection has led to the development of variable treatment options, with many more that are presently under trial. This review article discusses the pathogenesis of multiple organ involvement secondary to COVID-19 infection in infected patients.

Delayed hemodialysis in COVID-19: Case series with literature review.

BACKGROUND: Increased incidence of kidney injury has been seen in patients with COVID-19. However, less is known about COVID-19 susceptibility and outcomes in end-stage renal disease (ESRD) patients on hemodialysis (HD). Reduced angiotensin-converting enzyme 2 (ACE-2) from SARS-CoV-2 binding and increased angiotensin II (Ang-II) activity have been suggested as mechanisms for COVID-19 renal pathophysiology. MATERIALS AND METHODS: In this case series, we analyzed the data of 3 patients with ESRD who had a delay in receiving their regular HD. Reduced oxygen requirement, resolved hyperkalemia, and normalized fluid status were used for the basis of discharge. RESULTS: Presenting symptoms included fever, dyspnea, and dry cough. Laboratory markers were characteristic for COVID-19, such as lymphopenia, elevated D-dimer, C-reactive protein (CRP), and interleukin 6 (IL-6). All 3 of our reported patients required urgent HD upon admission. However, we report no fatalities in our case series, and our patients did not have a severe course of illness requiring endotracheal intubation. We reviewed COVID-19 pathophysiology and how patients with ESRD on HD may be particularly at risk for infection. CONCLUSION: New renal failure or ESRD sequelae, such as hyperkalemia, uremic encephalopathy, and fluid overload, can be exacerbated by a delay in receiving HD due to COVID-19 infection. Both direct COVID-19 infection and the challenges this pandemic creates to health care logistics present unique threats to ESRD patients on HD.

Ivabradine in Congestive Heart Failure: Patient Selection and Perspectives.

Heart failure (HF) is the fourth-most frequent cause of death and remains a challenge for public health. Therapy goals for HF with reduced ejection fraction (HFrEF) are the improvement in the quality of life, prolonged survival, a reduction of signs and symptoms, and the prevention of hospitalization. Angiotensin-converting enzyme inhibitors, beta-blockers, and mineralocorticoid receptor antagonists are the treatments of choice for HFrEF. Although ivabradine is not available in all countries, it is likely a new promising approach to improve outcomes in patients with HFrEF, either alone or with beta-blockers. Here, we review the current knowledge about ivabradine in HFrEF and assess its effect on outcomes in HF.

Carglumic Acid Treatment of a Patient with Recurrent Valproic Acid-induced Hyperammonemia: A Rare Case Report.

Valproic acid, first manufactured as an anticonvulsant, is commonly used to treat both neurological and psychiatric conditions. A rare and deadly side effect of this medication is hyperammonemia, presenting as lethargy, confusion, seizure, and, ultimately, coma. In rare circumstances, hyperammonemia can be recurrent and devastating, especially in patients with an underlying N-acetyl glutamate synthase (NAGS) deficiency, as the valproic acid can enhance this enzyme deficiency and inhibit the conversion of ammonia into urea in the liver. For these subtypes of patients, the United States Food and Drug Administration (US FDA) has recently approved carglumic acid, a medication that can act as a scavenger by effectively increasing the levels of NAGS, ultimately enhancing the conversion of ammonia to urea. In our case report, we have mentioned a patient with treatment-resistant bipolar disorder, who presented with elevated ammonia levels secondary to valproic acid treatment. Valproic acid was the only drug that was effective in his case, so we initiated therapy to reduce his elevated ammonia levels. After a thorough evaluation, we found the patient had a genetic NAGS deficiency. Carglumic acid was initiated and proved efficacious in our patient.

Pulmonary Involvement in Crohn's Disease: A Rare Case Report.

Crohn's disease (CD) is a granulomatous inflammatory disease that can involve any part of the gastrointestinal tract, from mouth to anus. In most cases, it remits and relapses in the terminal ileum, requiring treatment via steroid boluses. In rare cases, however, CD can involve the pulmonary system presenting as dyspnea on exertion and dry cough. We present a case of a 38-year-old man who developed shortness of breath, cough, and wheezing for one month after a colectomy procedure due to recurrent toxic megacolon. He recovered and tolerated extubation successfully and was prescribed mesalamine as maintenance therapy for CD. His pulmonary symptoms after the colectomy, along with his imaging and pulmonary function tests, indicated pulmonary involvement in the lungs as a progression of the primary inflammatory bowel disease. After confirming this diagnosis, he was treated with oral high-dose steroids after successful diagnosis, and the patient's symptoms improved dramatically. This case highlights often overlooked CD bronchopulmonary involvement in the postoperative period.

A Review of the Mechanism of Antagonism of N-methyl-D-aspartate Receptor by Ketamine in Treatment-resistant Depression.

The biochemical processes involved in depression go beyond serotonin, norepinephrine, and dopamine. The N-methyl-D-aspartate (NMDA) receptor has a major role in the neurophysiology of depression. Ketamine, one of the prototypical NMDA antagonists, works rapidly in controlling depressive symptoms, including acutely suicidal behavior, by just a single injection. Ketamine may rapidly increase the glutamate levels and lead to structural neuronal changes. Increased neuronal dendritic growth may contribute to synaptogenesis and an increase in brain-derived neurotrophic factor (BDNF). Activation of the mechanistic target of rapamycin (mTOR), as well as increased levels of BDNF, may increase long-term potentiation and result in an improvement in the symptoms of depression. The mechanisms of ketamine's proposed effect as an off-label treatment for resistant depression are outlined in this paper.

Diagnosis and Management of a Cardiac Amyloidosis Case Mimicking Hypertrophic Cardiomyopathy.

Cardiac amyloidosis is an acquired heart disease secondary to the deposition of ß-pleated amyloid proteins in heart tissue. Amyloid light chain (AL) amyloidosis is usually secondary to multiple myeloma and can rapidly deteriorate cardiac function, with high mortality. Up to 50% of AL patients have cardiac involvement presenting as heart failure, conduction abnormalities, and cardiomyopathies. One of the rare presentations is the likely simulation of disease with hypertrophic cardiomyopathies like left ventricular outflow tract (LVOT) obstruction due to the systolic anterior motion of the mitral valve and irregular septal hypertrophy secondary to amyloid deposits. We present a case of cardiac amyloidosis secondary to multiple myeloma who presented with dynamic LVOT obstruction resembling hypertrophic obstructive cardiomyopathy and complicated by acute pulmonary edema. These complicated cases can be initially treated for pulmonary edema with an elevation of the head of the bed, furosemide, and nitroglycerin intravenously. For multiple myeloma, chemotherapy was continued. Beta-blockers, calcium channel blockers and angiotensin-converting enzyme inhibitors, and aldosterone receptor blocker were avoided due to poor tolerability. After symptomatic control, the patient can likely be scheduled for septal myotomy and the placement of a pacemaker or implantable cardiac defibrillator to prevent any arrhythmias causing sudden cardiac death in these subsets of patients.