Postexercise hypotensive response in stroke patients following acute moderate or high intensity cycling session.

BACKGROUND: Hypertension is highly prevalent in stroke patients and reducing blood pressure is a priority. Aerobic exercise is known to induce postexercise hypotensive responses, but limited studies have documented this concept in stroke patients. The purpose was to investigate the effect of a single bout of moderate intensity continuous training (MICT) and high-intensity interval training (HIIT) on postexercise ambulatory blood pressure with patients with prior ischemic stroke or transient ischemic attack (TIA). METHODS: Ten hypertensive adults (mean age: 70±9 years) with prior ischemic stroke or TIA participated using a randomized crossover design. Ambulatory blood pressure was monitored for up to 8 hours after either ergocycle MICT or HIIT of respectively 50% and 95% of peak power output. Blood pressure was compared to pre-exercise resting measure. RESULTS: HIIT and MICT induced a decrease of systolic blood pressure of -11.0±9.2 mmHg and -4.7±4.5 mmHg respectively (P=0.03) immediately after the exercise. Ambulatory systolic blood pressure showed a steady linear increase (R2=0.90; P<0.001) of ~1.2 mmHg/hour and returned to pre-exercise measure after 8 hours. Effect of the two exercise conditions over time did not significantly differ (P=0.278). Diastolic blood pressure was not affected by both exercises. CONCLUSIONS: Those results suggest that HIIT induce a systolic blood pressure reduction of greater magnitude than MICT immediately after cycling exercise among patients with prior ischemic stroke or TIA. For both exercises, effects on ambulatory blood pressure are similar and persist up to 8 hours.

Urgent replacement of a mechanical mitral prosthesis in an anticoagulated patient with Bombay red blood cell phenotype.

PURPOSE: Bombay red blood cell phenotype is an extremely rare blood type for which patients can receive only autologous or Bombay phenotype red blood cells. We report a case of urgent repeat sternotomy for replacement of a mechanical mitral prosthesis in a patient with Bombay phenotype anticoagulated with warfarin, to emphasize the transfusion challenges in such patients. CLINICAL FEATURES: A male of Indian descent presented to hospital with New York Heart Association IV symptoms. His medical history revealed previous mitral valve replacement with a mechanical prosthesis in 2005 and Bombay phenotype blood. Preoperative transthoracic echocardiography demonstrated thrombus obstruction of the mitral prosthesis despite anticoagulation with warfarin. Right ventricular systolic pressure was >100 mmHg with 3+ tricuspid regurgitation. The patient's condition was temporized with diuretics, bronchodilators, and bi-level positive airway pressure ventilation while transfusion medicine and cardiac surgery were consulted for urgent surgery. The patient received vitamin K and prothrombin complex concentrate prior to repeat sternotomy and successful mitral prosthesis replacement. After cardiopulmonary bypass, heparinization was corrected with protamine and followed by a second dose of prothrombin complex concentrate and recombinant activated factor VIIa. Postoperatively, the patient received four units of packed red blood cells, two autologous units and two units of Bombay specific red blood cells. Right ventricular pressures stabilized at 40 mmHg following surgery. The patient recovered following several days of inotropic support with milrinone, diuretics, and bronchodilators. CONCLUSION: Patients with Bombay phenotype red blood cells present as type O, but they are unable to receive red blood cells from any phenotype other than Bombay phenotype. They are able to receive all other blood products, including fresh frozen plasma, cryoprecipitate, platelets, prothrombin complex concentrate, and recombinant activated factor VIIa. Coordination between Canadian Blood Services, transfusion medicine, surgery, and anesthesia is important in managing these patients.

Mobile ventricular thrombus arising from the mitral annulus in patients with dense mitral annular calcification.

Mitral annular calcification (MAC) has been considered a risk factor for thrombo-embolic disease. Superimposed thrombus formation on MAC has not been well described as a possible underlying mechanism for this association. We report three patients with mobile left ventricular (LV) thrombus arising from the LV aspect of severe calcified mitral annulus in the setting of normal LV function, mitral valve function, and sinus rhythm.