Impact of the COVID-19 Pandemic on Infective Endocarditis Management and Outcomes: Analysis of a National Clinical Database.

COVID-19 has widely affected health care delivery, but its impact on the management of infective endocarditis (IE), including valve surgery, is uncertain. We compared the national trends in admissions, demographics, and outcomes of IE before and after COVID-19 onset, using a national sample of IE admissions between 2016 and 2022 from the Vizient Clinical Database. The pre-COVID-19 and post-COVID-19 time periods were separated by the start of the second quarter of 2020, the time during which the COVID-19 pandemic was declared. For all admissions and for admissions involving valve surgery, pre-COVID-19 versus post-COVID-19 baseline characteristics and outcomes were compared using 2-sample t tests or chi-square tests. Propensity score-matched cohorts were similarly compared. Before COVID-19, there were 82,867 overall and 11,337 valve-related surgical admissions, and after COVID-19, there were 45,672 overall and 6,322 valve-related surgical admissions. In the matched analysis for all admissions, the in-hospital mortality increased from 11.4% to 12.4% after COVID-19 onset (p <0.001); in-hospital stroke (4.9% vs 6.0%, p <0.001), myocardial infarction (1.3% vs 1.4%, p = 0.03), and aspiration pneumonia (1.8% vs 2.4%, p <0.001) also increased, whereas other complications remained stable. In the matched analysis of surgical admissions, there was decreased in-hospital mortality (7.7% vs 6.7%, p = 0.03) and intensive care unit stay (8.5 ± 12.5 vs 8.0 ± 12.6 days, p = 0.04); other outcomes remained stable. In conclusion, patients admitted with IE after COVID-19 were more medically complex with worsened outcomes and mortality, whereas patients who underwent valve surgery had stable outcomes and improved mortality despite the pandemic.

mTOR inhibition prevents angiotensin II-induced aortic rupture and pseudoaneurysm but promotes dissection in Apoe-deficient mice.

Aortic dissection and rupture are triggered by decreased vascular wall strength and/or increased mechanical loads. We investigated the role of mTOR signaling in aortopathy using a well-described model of angiotensin II-induced dissection, aneurysm, or rupture of the suprarenal abdominal aorta in Apoe-deficient mice. Although not widely appreciated, nonlethal hemorrhagic lesions present as pseudoaneurysms without significant dissection in this model. Angiotensin II-induced aortic tears result in free rupture, contained rupture with subadventitial hematoma (forming pseudoaneurysms), dilatation, or healing, while the media invariably thickens regardless of mural tears. Medial thickening results from smooth muscle cell hypertrophy and extracellular matrix accumulation, including matricellular proteins. Angiotensin II activates mTOR signaling in vascular wall cells, and inhibition of mTOR signaling by rapamycin prevents aortic rupture but promotes dissection. Decreased aortic rupture correlates with decreased inflammation and metalloproteinase expression, whereas extensive dissection correlates with induction of matricellular proteins that modulate adhesion of vascular cells. Thus, mTOR activation in vascular wall cells determines whether aortic tears progress to dissection or rupture. Previous mechanistic studies of aortic aneurysm and dissection by angiotensin II in Apoe-deficient mice should be reinterpreted as clinically relevant to pseudoaneurysms, and mTOR inhibition for aortic disease should be explored with caution.

Robotic Transthoracic Repair of a Right-Sided Traumatic Diaphragmatic Rupture.

Introduction Traumatic diaphragm rupture injury repairs are predominately performed through thoracotomy, laparotomy, or a combination of the two approaches. While open surgery is often necessary to follow the fundamentals of damage-control operations in unstable or polytrauma patients, minimally invasive surgery may be an alternative for those with a low injury burden to reduce the postoperative morbidities associated with open operations. Case Description We describe the first case of a right-sided diaphragm rupture from blunt trauma that was repaired by a robotic transthoracic approach in the index admission. Conclusion Minimally invasive repair of an acute traumatic diaphragm rupture is feasible in selected trauma patients.

Interrupted aortic arch with post-interruption aneurysm and bicuspid aortic valve in an adult: a case report and literature review.

Interrupted aortic arch in adults is rare with a limited number of reported cases. We describe a case of a 53-year-old woman with interrupted aortic arch, bicuspid aortic valve, and post-interruption saccular aneurysm of the aorta. To our knowledge, this is only the second report of an adult patient with all 3 abnormalities. We also review the literature on this unusual condition and discuss its relationship with coarctation of the aorta.

Unicuspid unicommissural aortic valve: an extremely rare congenital anomaly.

Unicuspid aortic valve is a rare congenital malformation that usually presents in the 3rd to 5th decade of life-and usually with severe aortic stenosis or regurgitation. It often requires surgical correction. Diagnosis can be made with 2- or 3-dimensional transthoracic or transesophageal echocardiography, cardiac computed tomography, or cardiac magnetic resonance imaging. We report the case of a 31-year-old man who presented with dyspnea on exertion due to severe aortic stenosis secondary to a unicuspid unicommissural aortic valve. After aortic valve replacement, this patient experienced complete heart block that required the placement of a permanent pacemaker.

Innominate artery injury from disseminated tuberculosis.

A 49-year-old man presented with chest pain and was found to have hemorrhage and drainage from a chest wound secondary to disseminated tuberculosis involving the sternum and ankle. He then developed acute hemorrhage from an innominate artery pseudoaneurysm originating just below a severely diseased sternoclavicular junction. A staged approach was used to manage his pathology given the life-threatening bleeding and his debilitated condition. He underwent endovascular stent grafting to exclude the pseudoaneurysm, followed by aggressive debridement of the affected sternal area.

An intriguing co-existence: atrial myxoma and cerebral cavernous malformations: case report and review of literature.

It is commonly postulated that neurologic complications of atrial myxomas are due to either direct tumor embolization or mycotic aneurysm of cerebral vasculature or rupture of mycotic aneurysms of cerebral arteries. However, the authors report the case of 63-year-old woman with a large left atrial myxoma whose progressive left-sided weakness was due to a different neurologic mechanism, namely, multiple bleeding cavernous malformations, which were visualized by magnetic resonance imaging of the brain. Cerebral cavernous malformations coexist with mesenchymal anomalies of other organs, including the liver, kidneys, and retinas. To the best of the authors' knowledge, this is only the second reported case of coexistent cerebral cavernous malformations and atrial myxoma.

Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms.

BACKGROUND: Progressive medial degeneration and atrophy is thought to be a cause of ascending thoracic aortic aneurysms in the elderly. Extensive apoptosis of vascular smooth muscle cells (VSMCs) has been demonstrated in the media of abdominal aortic aneurysms. We investigated whether medial atrophy from loss of VSMCs occurs in primary ascending thoracic aortic aneurysms. METHODS AND RESULTS: Morphometric analysis of 28 nonaneurysmal ascending thoracic aortas and 29 ascending thoracic aortic aneurysms was performed by directly measuring the thickness of their vascular layers and by indirectly calculating the area of their vascular compartments. The cellular and matrix composition of the media was assessed at the structural, protein, and transcript levels. Despite thinning of the media secondary to vascular dilatation, there was an overall increase in the medial area of aneurysms. VSMC density was preserved, implying cellular hyperplasia as a result of the increased medial mass. There was decreased expression of matrix proteins, despite sustained synthesis of these molecules, which was associated with evidence of increased matrix degradation. The remodeling and expansion of the media was most evident in comparisons between nonaneurysmal aortas versus smaller aneurysms and did not evolve further in larger aneurysms. CONCLUSIONS: The mechanisms for luminal enlargement in thoracic and abdominal aortic aneurysms differ significantly with regard to the survival of VSMCs and atrophy of the media but share common pathophysiology involving degeneration of the matrix. Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms may be an initial adaptive response to minimize increased wall stress resulting from vascular dilatation.

Right ventricle-sparing heart transplantation effective against iatrogenic pulmonary hypertension.

BACKGROUND: Right heart failure is the predominant cause of death following heart transplantation, occurring with disturbingly high frequency in patients with severe antecedent pulmonary hypertension. We have recently reported a novel technique of heart transplantation that spares the recipient right ventricle, excising only the recipient left ventricle. The resulting model has 2 right hearts and 1 left heart. The aim is to preserve the recipient's right ventricle, which is already conditioned to pulmonary hypertension. The hope is that, in this way, death due to right heart failure can be prevented in humans. Our prior report was a feasibility study in normal dogs. This study challenges this new technique by creating iatrogenic pulmonary hypertension in the recipient animals. METHODS: Iatrogenic pulmonary hypertension was created in 4 recipient canines by intravenous injection of the pulmonary toxin monocrotaline pyrrole (single bolus of 3.5 to 4.5 mg/kg intravenously [i.v.]). RESULTS: Within 6 weeks of monocrotaline administration, relative pulmonary hypertension occurred (mean pulmonary artery [PA] pressure 20 mm Hg vs 10 mm Hg for controls [p < 0.01]) (pulmonary vascular resistance [PVR] 4.2 vs 1.5 Wood units [P < 0.01]), and right ventricular (RV) hypertrophy developed (RV thickness 11 mm vs 2 mm [P < 0.04]). Histologic examination confirmed severe muscle infiltration and thickening of the media of the pulmonary arterioles. RV-sparing heart transplantation was performed successfully in all 4 animals with pulmonary hypertension. In all cases, the animals were weaned without difficulty from cardiopulmonary bypass, despite the ambient pulmonary hypertension, on low-dose epinephrine, maintaining systolic blood pressure of 104 mm Hg at right atrial pressure of 7 mm Hg. Both right hearts contracted well without dilation or strain. A single "control" traditional orthotopic transplant experiment in an animal with monocrotaline-induced pulmonary hypertension resulted in immediate death from right heart failure. CONCLUSIONS: Right ventricle-sparing heart transplantation ("one-and-one-half heart model") can handle pulmonary hypertension without difficulty. This evidence adds impetus for further pursuing of right ventricle-sparing heart transplantation to decrease the incidence of death from right heart failure in recipients with severe antecedent pulmonary hypertension.

Aortic arch replacement for recurrent cerebral embolization.

Replacement of the aortic arch for atheroma with cerebral embolization is in its infancy. The appropriateness of such intervention is controversial. Over a 10-month period, a 58-year-old woman suffered multiple debilitating cerebral vascular accidents manifested by motor, sensory, and memory deficits and documented by computed tomographic scanning and magnetic resonance imaging. Carotid and vertebral arteries were free of arteriosclerotic disease. Transesophageal echocardiography demonstrated two large atheromas with friable, pedunculated forms, one in the aortic arch and one in the very proximal descending thoracic aorta. Transcranial ultrasound revealed recurrent cerebral microembolic events. Cerebrovascular events continued, and the atheromas increased in size, despite treatment with Coumadin and aspirin. Under deep hypothermic arrest, the segment of the aortic arch harboring the atheroma was excised and replaced with a Dacron graft. Repeat transcranial ultrasound revealed cessation of embolic signals. All cerebrovascular events ceased. No further anticoagulation therapy was required. The patient has made substantial recovery from the preoperative deficits and continues to do well 1 year after aortic arch replacement. Resection of mobile aortic arch atheromas is likely to become increasingly important in the future as transesophageal echocardiography leads to their more common identification as a cause of cerebral ischemic events.