A schedule for tapering glucocorticoid treatment in patients with severe SARS-CoV 2 infection can prevent acute adrenal insufficiency in the geriatric population.

OBJECTIVE AND DESIGN: Glucocorticoids (GCs) have been widely used in symptomatic patients for the treatment of COVID-19. The risk for adrenal insufficiency must be considered after GC withdrawal given that it is a life-threatening condition if left unrecognized and untreated. Our study aimed to diagnose adrenal insufficiency early on through a GC reduction schedule in patients with COVID-19 infection. PATIENTS AND MEASUREMENTS: From November 2021 to May 2022, 233 patients were admitted to the Geriatric Division of the University Hospital of Padova with COVID-19 infection. A total of 122 patients were treated with dexamethasone, after which the GC tapering was performed according to a structured schedule. It consists of step-by-step GC tapering with prednisone, from 25 mg to 2.5 mg over 2 weeks. Morning serum sodium, potassium, and cortisol levels were assessed 3 days after the last dose of prednisone. RESULTS: At the end of GC withdrawal, no adrenal crisis or signs/symptoms of acute adrenal insufficiency were reported. Median serum cortisol, sodium, and potassium levels after GC discontinuation were, respectively, 427 nmol/L, 140 nmol/L, and 4 nmol/L (interquartile range 395-479, 138-142, and 3.7-4.3). A morning serum cortisol level below the selected threshold of 270 nmol/L was observed in two asymptomatic cases (respectively, 173 and 239 nmol/L, reference range 138-690 nmol/L). Mild hyponatremia (serum sodium 132 to 134 nmol/L, reference range 135-145 nmol/L) was detected in five patients, without being related to cortisol levels. CONCLUSIONS: A structured schedule for the tapering of GC treatment used in patients with severe COVID-19 can reduce the risk of adrenal crisis and acute adrenal insufficiency.

Acute coronary syndrome and diabetic keto acidosis: the chicken or the egg?

We sought to describe two cases of diabetic ketoacidosis (DKA) with elevated troponin. The association of DKA with myocardial infarction (MI) is very frequent. We therefore decide to look deeply in the potential mechanisms behind this strong relationship. We did review the potential role of severe acidosis, intracellular calcium, the counter-regulatory hormones and the potential of the free fatty acid release. Those two conditions can trigger each other and it is often difficult to know which condition appear first. Ultimately, it stands to reason that the message for the clinician should be that a troponin elevation in a DKA patient should always be considered as a coronary abnormality until proven otherwise.

Cardiogenic Shock after Nifedipine Administration in a Pregnant Patient: A Case Report and Review of the Literature.

We present a case of a 21-year-old Caucasian woman at 27 weeks of pregnancy who was admitted to the obstetric department for pre-term labor. She received 10 mg of nifedipine 4 times in 1 h, according to the internal protocol. Shortly after, she brutally deteriorated with pulmonary edema and hypoxemia requiring transfer to the intensive care unit (ICU) for mechanical ventilation. She finally improved and was successfully extubated after undergoing a percutaneous valvuloplasty of the mitral valve. This case illustrates a severe cardiogenic shock after administration of nifedipine for premature labor in a context of unknown rheumatic mitral stenosis. Nifedipine induces a reflex tachycardia that reduces the diastolic period and thereby precipitates pulmonary edema in case of mitral stenosis. This case emphasizes the fact that this drug may be severely harmful and should never be used before a careful physical examination and echocardiography if valvular heart disease is suspected.

Myocardial mechano-energetic efficiency in hypertensive adults.

BACKGROUND: Myocardial mechanical efficiency can be measured as the ratio between systolic work and energy consumption. We evaluated the relation between myocardial mechanical efficiency and left ventricular (LV) mass in untreated hypertensive patients. METHODS: Myocardial work was estimated in 256 normotensive (35 +/- 12 years) and 306 hypertensive patients (47 +/- 10 years) with normal ejection fraction, as stroke work in gram-meters (stroke work = BPs x SV x 0.0144, where BPs is systolic blood pressure, SV is echocardiographic stroke volume). Myocardial O2 consumption was estimated as the product of heart rate (HR) x BPs (eMVO2). Myocardial mechanical efficiency was estimated as the ratio of stroke work/eMVO2, which can be simplified and expressed as ml/s. RESULTS: LV mass was greater in hypertensive than in normotensive patients (46 +/- 13 vs. 38 +/- 11 g/m2.7, P < 0.0001), but myocardial mechanical efficiency was identical (85 +/- 23 vs. 86 +/- 26 ml/s). Relations between myocardial mechanical efficiency and LV mass were close (both P < 0.0001), but more scattered among hypertensive patients because of 56 patients exhibiting low myocardial mechanical efficiency relative to the magnitude of LV mass. At comparable age and body size, these patients had higher HR, BPs, and pulse pressure than those with normal myocardial mechanical efficiency (all P < 0.001). After adjusting for age and sex, hypertensive patients with low myocardial mechanical efficiency showed greater relative wall thickness and lower ejection fraction and midwall shortening than those with normal myocardial mechanical efficiency (all P < 0.001). Low myocardial mechanical efficiency was also associated with inappropriately high LV mass (P < 0.0001). CONCLUSION: In some hypertensive patients the left ventricle works inefficiently with a high energy wasting, at the same level of LV mass as hypertensive patients with normal myocardial mechanical efficiency. Those patients feature a high cardiovascular risk phenotype, with concentric LV geometry, systolic dysfunction, and indirect signs of more severe vascular impairment.