Mid to Late Life Hypertension Trends and Cerebral Small Vessel Disease in the Framingham Heart Study.

The duration and lifetime pattern of hypertension is related to risk of stroke and dementia. In turn, cerebral small vessel disease (CSVD) is the most frequent form of cerebrovascular disease underlying dementia and stroke. Thus, study of the relation of mid to late life hypertension trends with CSVD late in life will help understand hypertension's role and inform preventive efforts of CSVD consequences. We studied 1686 Framingham Heart Study Offspring cohort participants free of stroke and dementia, who were examined in mid and late life, and had available brain magnetic resonance imaging during late life. We related hypertension trends between mid and late life (normotension-normotension N-N, normotension-hypertension N-H, hypertension-hypertension H-H) to cerebral microbleeds and covert brain infarcts (CBI), overall and stratified by brain topography. We used multivariable logistic regression analyses to calculate odds ratio and 95% CIs for CSVD measures. The prevalence of CSVD in late life was 8% for cerebral microbleeds and 13% for covert brain infarcts and increased with longer hypertension exposure across all brain regions. Compared with the trend pattern of N-N, both N-H and H-H trends had higher odds of mixed cerebral microbleeds (2.71 [1.08-6.80], and 3.44 [1.39-8.60], respectively); H-H also had higher odds of any cerebral microbleeds or covert brain infarcts (1.54 [1.12-2.20]), and any covert brain infarcts (1.55 [1.08-2.20]). The burden of CSVD also increased with longer hypertension exposure. Our results highlight hypertension having a major role in subclinical CSVD, across subtypes and brain regions, and call attention to improve recognition and treatment of hypertension early in life.

Acute stroke, catheter related venous thrombosis, and paradoxical cerebral embolism: report of two cases.

BACKGROUND: Patent foramen ovale (PFO) has been associated with cryptogenic stroke, particularly in young adults. However, the source of particles leading to cerebral embolism remains frequently unknown despite comprehensive evaluation. OBJECTIVE: To report and comment on therapeutic options for 2 patients with acute ischemic strokes, PFO, and venous access related thrombosis, sources of paradoxical embolism, from Boston Medical Center stroke database. CASE DESCRIPTIONS: Case 1. A 71-year-old man presented with brain magnetic resonance imaging (MRI) confirmed acute cerebellar infarction. Echocardiography showed a PFO and thrombotic material at the tip of a peripherally inserted central catheter (PICC) line in the superior vena cava (SVC) prolapsing into the right atrium (RA). Case 2. A 64-year-old woman with end-stage renal disease and PFO presented with brain MRI confirmed acute parietal lobe infarction. Three days prior to her stroke, she had thrombectomy and venoplasty of an arterio-venous (AV) dialysis graft followed by a post-thrombectomy fistulogram that showed persistent thrombotic material at the venous site. CONCLUSIONS: PFO associated with large venous access site thrombosis was the most likely mechanism of stroke in both cases. Local thrombosis at sites of large venous access may be an overlooked source of paradoxical embolism in patients with PFO as well as a preventable cause of stroke in critically ill patients.