Killip scale reclassification according to lung ultrasound: Killip pLUS.

AIMS: The Killip scale remains a fundamental tool for prognostic assessment in ST-segment elevation myocardial infarction (STEMI) due to its simplicity and predictive value. Lung ultrasound (LUS) has emerged as a valuable adjunct for diagnosing and predicting outcomes in heart failure (HF) and STEMI patients, even those with subclinical congestion. We created a new classification (Killip pLUS), which reclassifies Killip I and II patients into an intermediate category (Killip I pLUS) based on LUS results. This category included Killip I patients and ≥1 positive zone (≥3 B-lines) and Killip II with 0 positive zones. We aimed to evaluate this new classification by comparing it with the Killip scale and a previous LUS-based reclassification scale (LUCK scale). METHODS AND RESULTS: Lung ultrasound was performed within 24 h of admission in a multicentre cohort of 373 patients admitted for STEMI. In-hospital mortality and major adverse cardiovascular events within one year after admission, comprising mortality or readmission for HF, acute coronary syndrome, or stroke, were analysed. When predicting in-hospital mortality, the global comparison of these three classifications was statistically significant: Killip pLUS area under the curve (AUC) 0.90 (95% CI 0.85-0.95) vs. Killip AUC 0.85 (95% CI 0.73-0.96) vs. LUCK 0.83 (95% CI 0.70-0.95), P = 0.024. To predict events during follow-up, the comparison between scales was also significant: Killip pLUS 0.77 (95% CI 0.71-0.85) vs. Killip 0.72 (95% CI 0.65-0.79) vs. LUCK 0.73 (95% CI 0.66-0.81), P = 0.033. CONCLUSION: The Killip pLUS scale provides enhanced risk stratification compared to the Killip and LUCK scales while preserving simplicity.

Subclinical congestion assessed by lung ultrasound in ST segment elevation myocardial infarction.

OBJECTIVE: We evaluated the prognostic value of subclinical congestion assessed by lung ultrasound (LUS) in patients admitted for ST segment elevation myocardial infarction (STEMI). METHODS: This was a multicentre study that prospectively enrolled 312 patients admitted for STEMI without signs of heart failure (HF) at admission. LUS was performed during the first 24 hours after revascularisation and classified patients as having either wet lung (three or more B-lines in at least one lung field) or dry lung. The primary endpoint was a composite of acute HF, cardiogenic shock or death during hospitalisation. The secondary endpoint was a composite of readmission for HF or new acute coronary syndrome or death during 30-day follow-up. Zwolle score was calculated in all patients to assess predictive improvement by adding the result of the LUS to this score. RESULTS: 14 patients (31.1%) in the wet lung group presented the primary endpoint vs 7 (2.6%) in the dry lung group (adjusted RR 6.0, 95% CI 2.3 to 16.2, p=0.007). The secondary endpoint occurred in five patients (11.6%) in the wet lung group and in three (1.2%) in the dry lung group (adjusted HR 5.4, 95% CI 1.0 to 28.7, p=0.049). Addition of LUS improved the ability of the Zwolle score to predict the follow-up composite endpoint (net reclassification improvement 0.99). LUS showed a very high negative predictive value in predicting in-hospital and follow-up endpoints (97.4% and 98.9%, respectively). CONCLUSION: Early subclinical pulmonary congestion identified by LUS in patients with Killip I STEMI at hospital admission is associated with adverse outcomes during hospitalisation and 30-day follow-up.

Myocardial Injury in COVID-19 and Its Implications in Short- and Long-Term Outcomes.

COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is still a pandemic with high mortality and morbidity rates. Clinical manifestation is widely variable, including asymptomatic or mild respiratory tract illness to severe pneumonia and death. Myocardial injury is a significant pathogenic feature of COVID-19 and it is associated with worse in-hospital outcomes, mainly due to a higher number of hospital readmissions, with over 50% mortality. These findings suggest that myocardial injury would identify COVID-19 patients with higher risk during active infection and mid-term follow-up. Potential contributors responsible for myocardial damage are myocarditis, vasculitis, acute inflammation, type 1 and type 2 myocardial infarction. However, there are few data about cardiac sequelae and its long-term consequences. Thus, the optimal screening tool for residual cardiac sequelae, clinical follow-up, and the benefits of a specific cardiovascular therapy during the convalescent phase remains unknown. This mini-review explores the different mechanisms of myocardial injury related to COVID-19 and its short and long-term implications.

Tratamiento de la pericarditis aguda recidivante guiado por resonancia magnética / Magnetic resonance-guided treatment for recurrent pericarditis

No disponible