'Here comes the story of the Hurricane': a case report of AL cardiac amyloidosis and myocardial bridging.

Background: Cardiac amyloidosis (CA) is a rapidly progressive infiltrative cardiomyopathy, whose role is emerging as a not-so-rare disorder leading to heart failure (HF). Myocardial bridge (MB) is the most common inborn coronary artery variant, and its clinical relevance is still matter of debate. The exceptional coexistence of these two conditions could accelerate disease progression and worsen the already compromised clinical conditions. Case summary: We present the case of a 76-year-old female patient experiencing relapsing HF decompensation and presenting to our centre with dyspnoea at rest and severe peripheral congestion. Echocardiogram showed severe concentric hypertrophy, severe biventricular contractile dysfunction, and third-degree diastolic dysfunction. Coronary angiography excluded epicardial atherosclerotic disease, though displaying a long intramyocardial course of left anterior descending artery. Physiological invasive test was achieved in terms of instantaneous wave-free ratio (iFR), both at baseline and after inotropic and chronotropic stimuli, and attested haemodynamic significance. Concurrently, the diagnostic flow chart for CA was accomplished, by means of both invasive (periumbilical fat biopsy, bone marrow aspiration) and non-invasive tests (99mTc-diphosphonate scintigraphy, serum-urine immunofixation) that confirmed the suspect of primary amyloidosis. Acute HF therapy was personalized according to the singularity of the case, avoiding both nitrates and beta-blockers, then first cycle of chemotherapy was started. Discussion: Our clinical case shows a unique interaction between infiltrative cardiomyopathy and coronary artery abnormality. Amyloidosis can contribute to the ischaemic burden of the MB and this may, in turn, abbreviate the path to HF decompensation.

2019 novel Coronavirus: current knowledge, cardiovascular implications and management.

From first cases reported on December 31, 2019, in Wuhan, Hubei-China, SARS-CoV2 has spread worldwide and finally the World Health Organization declared the pandemic status. We summarize what makes SARS-CoV2 different from previous highly pathogenic coronaviruses and why it is so contagious, with focus on its clinical presentation and diagnosis, which is mandatory to start the appropriate management and reduce the transmission. As far as infection pathophysiology is still not completely clarified, this review focuses also on the cardiovascular (CV) implication of COVID-19 and the capability of this virus to cause direct myocardial injury, myocarditis and other CV manifestations. Furthermore, we highlight the relationship between the virus, enzyme ACE2 and ACE inhibitors. Clinical management involves the intensive care approach with intubation and mechanical ventilation in the most serious cases and drug therapy with several apparently promising old and new molecules. Aim of this review is then to summarize what is actually known about the SARS-CoV2 and its cardiovascular implications.

Prevalence and characteristics of myocardial injury during COVID-19 pandemic: A new role for high-sensitive troponin.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is a pandemic disease that is causing a public health emergency. Characteristics and clinical significance of myocardial injury remain unclear. METHODS: This retrospective single-center study analyzed 189 patients who received a COVID-19 diagnosis out of all 758 subjects with a high sensitive troponin I (Hs-TnI) measurement within the first 24 h of admission at the Policlinico A.Gemelli (Rome, Italy) between February 20th 2020 to April 09th 2020. RESULTS: The prevalence of myocardial injury in our COVID-19 population is of 16%. The patients with cardiac injury were older, had a greater number of cardiovascular comorbidities and higher values of acute phase and inflammatory markers and leucocytes. They required more frequently hospitalization in Intensive Care Unit (10 [32.3%] vs 18 [11.4%]; p = .003) and the mortality rate was significantly higher (17 [54.8%] vs. 15 [9.5%], p < .001). Among patients in ICU, the subjects with myocardial injury showed an increase need of endotracheal intubation (8 out of 9 [88%] vs 7 out of 19[37%], p = .042). Multivariate analyses showed that hs-TnI can significantly predict the degree of COVID-19 disease, the intubation need and in-hospital mortality. CONCLUSIONS: In this study we demonstrate that hs-Tn can significantly predict disease severity, intubation need and in-hospital death. Therefore, it may be reasonable to use Hs-Tn as a clinical tool in COVID-19 patients in order to triage them into different risk groups and can play a pivotal role in the detection of subjects at high risk of cardiac impairment during both the early and recovery stage.

Stay Home! Stay Safe! First Post-Discharge Cardiologic Evaluation of Low-Risk-Low-BNP Heart Failure Patients in COVID-19 Era.

BACKGROUND: The COVID-19 pandemic has had a deep impact on periodic outpatient evaluations. The aim of this study was to evaluate the impact of low brain natriuretic peptide (BNP) values in predicting adverse events in heart failure (HF) patients in order to evaluate implications for safe delay of outpatient visits. METHODS: This was a retrospective study. One-thousand patients (mean age: 72 ± 10 years, 561 women) with HF and BNP values <250 pg/mL at discharge were included. A 6-month follow-up was performed. The primary endpoint was a combination of deaths and readmissions for HF within 6-month after discharge. RESULTS: At 6-month follow-up, 104 events (10.4%) were recorded (65 HF readmissions and 39 all-cause deaths). Univariate Cox analysis identified as significant predictors of outcome were age (p < 0.001, hazard ratio [HR] = 1.044), creatinine (p = 0.001, HR = 1.411), and BNP (p < 0.001, HR = 1.010). Multivariate Cox regression confirmed that BNP (p < 0.001, HR = 1.009), creatinine (p = 0.016, HR = 1.247), and age (p = 0.013, HR = 1.027) were independent predictors of events in HF patients with BNP values <250 pg/mL at discharge. Patients with BNP values >100 pg/mL and creatinine >1.0 mg/dL showed increased events rates (from 4.3% to 19.0%) as compared to those with lower values (p < 0.000, HR = 4.014). CONCLUSIONS: Low pre-discharge BNP levels were associated with low rates of cardiovascular events in HF patients, independently of the frequency of follow-up.

A nontrivial differential diagnosis in COVID-19 pandemic: a case report and literary review of amiodarone-induced interstitial pneumonia.

Amiodarone is a drug commonly used to treat and prevent cardiac arrhythmias, but it is often associated with several adverse effects, the most serious of which is pulmonary toxicity. A 79-year-old man presented with respiratory failure due to interstitial pneumonia during the COVID-19 pandemic. The viral etiology was nevertheless excluded by repeated nasopharyngeal swabs and serological tests and the final diagnosis was amiodarone-induced organizing pneumonia. The clinical and computed tomography findings improved after amiodarone interruption and steroid therapy. Even during a pandemic, differential diagnosis should always be considered and pulmonary toxicity has to be taken into account in any patient taking amiodarone and who has new respiratory symptoms.

2019 novel-coronavirus: Cardiovascular insights about risk factors, myocardial injury, therapy and clinical implications.

From December 31st, 2019, a novel highly pathogenic coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread worldwide, reaching at present the dimension of a pandemic. In addition to damaging the lungs, SARS-CoV-2 may also damage the heart and this is corroborated by the evidence that cardiovascular comorbidities are associated with a higher mortality and poor clinical outcomes in patient infected by the virus. During the infection myocardial injury, myocarditis and arrhythmias have also been reported, but the pathophysiological mechanisms of these complications are yet to be understood. Great attention is also being posed on the potential beneficial/harmful role of angiotensin converting enzyme (ACE) inhibitors, as far as the virus binds to ACE2 to infect cells, but evidences lack. Furthermore, SARS-CoV-2 can also affect the aspect of acute coronary syndromes, not only because these two distinct pathological entities share pathogenic aspects (such as the systemic inflammatory state and cytokine release), but also and above all for the consequences that the need to contain the infection has on the management of cardiological urgencies. The aim of this review was therefore to summarize the relationship between the virus and the cardiovascular system.

2019 novel Coronavirus: current knowledge, cardiovascular implications and management.

From first cases reported on December 31, 2019, in Wuhan, Hubei-China, SARS-CoV2 has spread worldwide and finally the World Health Organization declared the pandemic status. We summarize what makes SARS-CoV2 different from previous highly pathogenic coronaviruses and why it is so contagious, with focus on its clinical presentation and diagnosis, which is mandatory to start the appropriate management and reduce the transmission. As far as infection pathophysiology is still not completely clarified, this review focuses also on the cardiovascular (CV) implication of COVID-19 and the capability of this virus to cause direct myocardial injury, myocarditis and other CV manifestations. Furthermore, we highlight the relationship between the virus, enzyme ACE2 and ACE inhibitors. Clinical management involves the intensive care approach with intubation and mechanical ventilation in the most serious cases and drug therapy with several apparently promising old and new molecules. Aim of this review is then to summarize what is actually known about the SARS-CoV2 and its cardiovascular implications.