Abstract-A link between oral health and cardiovascular disease has been proposed for more than a century. Recently, concern about possible links between periodontal disease (PD) and atherosclerotic vascular disease (ASVD) has intensified and is driving an active field of investigation into possible association and causality. The 2 disorders share several common risk factors, including cigarette smoking, age, and diabetes mellitus. Patients and providers are increasingly presented with claims that PD treatment strategies offer ASVD protection; these claims are often endorsed by professional and industrial stakeholders. The focus of this review is to assess whether available data support an independent association between ASVD and PD and whether PD treatment might modify ASVD risks or outcomes. It also presents mechanistic details of both PD and ASVD relevant to this topic. The correlation of PD with ASVD outcomes and surrogate markers is discussed, as well as the correlation of response to PD therapy with ASVD event rates. Methodological issues that complicate studies of this association are outlined, with an emphasis on the terms and metrics that would be applicable in future studies. Observational studies to date support an association between PD and ASVD independent of known confounders. They do not, however, support a causative relationship. Although periodontal interventions result in a reduction in systemic inflammation and endothelial dysfunction in short-term studies, there is no evidence that they prevent ASVD or modify its outcomes. (Circulation. 2012;125:2520-2544.)

Rectus sheath hematoma (RSH) is a known complication of anticoagulation therapy and a source of potential morbidity and mortality. Early diagnosis and appropriate treatment may help to prevent complications including hemodynamic instability, the abdominal compartment syndrome or multiorgan dysfunction. Although the diagnosis can be made clinically, it can be confirmed with computed tomography of the abdomen. Most patients can be managed conservatively; however, it is often necessary to suspend anticoagulation in the acute setting. Rectus sheath hematoma is not a contraindication to resuming anticoagulation once the hematoma has been adequately managed and the patient has returned to a stable clinical baseline.

Some patients need higher-than-expected doses of warfarin (Coumadin) to get their international normalized ratio (INR) into the therapeutic range. The cause of warfarin resistance can be either acquired (eg, poor compliance, drug interactions, dietary interactions) or hereditary, but the genetic mechanisms of warfarin resistance are not well understood. This review offers an algorithm for the evaluation of patients with suspected warfarin resistance.

Venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism, represents a significant source of morbidity and mortality. It is readily diagnosed with noninvasive modalities when there is a clinical suspicion. Most patients presenting with signs and symptoms of DVT have well-known risk factors, such as a history of VTE, malignancy, recent illness, or immobilization. A subset of individuals with idiopathic VTE have no readily identifiable risk factors. Therapeutic anticoagulation is the cornerstone of management in all patients with VTE. Adjunctive measures, such as thrombolysis and the use of vena cava filters, are indicated in select cases. The ideal duration of anticoagulation is unknown, but is often maintained long-term in patients with acquired or inherited thrombophilia. Warfarin is the only oral anticoagulant approved by the US Food and Drug Administration. Warfarin carries a substantial annual risk of bleeding complications, requires ongoing monitoring, and has extensive drug-drug interactions, which are causes for concern in patients requiring long-term anticoagulation. Alternative oral anticoagulants, such as direct thrombin inhibitors and factor Xa inhibitors, are subjects of active research in alternative agents for oral anticoagulation, and have been recently approved for prophylaxis in Canada and the European Union.

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Descending thoracic aortic aneurysms, similar to other aneurysms, are often incidentally diagnosed in patients with unrelated complaints. Management of these aneurysms is largely dependent on their size and anatomy. Most individuals with asymptomatic descending thoracic aortic aneurysms may be safely managed with cardiovascular risk factor modification until the aneurysm size reaches 6 cm. A subset of individuals, such as those whose descending thoracic aortic aneurysm measures > 6 cm or in cases of rapid growth, should be offered repair, increasingly performed via an endovascular approach. The higher risk of aneurysm rupture in women poses a unique consideration, although to date no gender-specific consensus screening guideline exists for aneurysmal disease of the thoracic aorta.

A 29-year-old woman with a history of systemic lupus erythematosus (SLE) presented to our medical center with 9 days of worsening left wrist and hand cellulitis and ulceration unresponsive to broad-spectrum antibiotics including cefepime, linezolid, and ciprofloxacin (Panel A). Concurrent immune modulation therapy included pulse dose methylprednisolone. Prior to hospitalization she was on maintenance dose hydroxychloroquine for SLE.In addition to concern of infection, vasculitic and thrombotic etiologies were also entertained. Both arterial and venous imaging studies were unremarkable. Given her unresponsiveness to broad-spectrum antibiotics and immune modulation therapy, a skin biopsy was obtained.