Introduction hypertension is the most common cardiac disease in Nigeria. There are very limited studies in Nigeria on the use of 24-hour ambulatory blood pressure monitoring (24-h ABPM) for evaluation of hypertensive patients. Twenty four-hour ABPM, unlike office blood pressure (OBP), can assess diurnal variation using parameters like awake blood pressure (BP), asleep (nocturnal) BP, mean 24-hour BP and dipping pattern. This can help in assessment of increased cardiovascular risk and management of hypertensive patients. We purposed to assess the diurnal rhythm of BP among Nigerians with hypertension. Methods this was a prospective cross-sectional study. Consecutive 77 hypertensive subjects were studied using Schiller MT-300 for 24-h ABPM. Results out of the 77 patients reviewed, 39 (50.6%) were females. The mean age was 50.9 years (SD 13.5). The mean awake systolic and diastolic BP were 135.6mmHg (SD 15.0) and 83.2mmHg (SD 10.0) respectively; mean asleep systolic and diastolic BP were 127.6mmHg (SD 17.9) and 76.2mmHg (SD 12.2) respectively; and mean 24-h systolic and diastolic BP were 133.6mmHg (SD 15.3) and 81.4mmHg (SD 10.2) respectively. Awake BP was elevated in 59.7% of study subjects. Elevated awake systolic BP and awake diastolic BP were present in 50.6% and 41.6% of the study population. Nocturnal (asleep) BP was elevated in 79.2%. Non-dipping pattern was the most prevalent pattern at 55.8%, followed by dipping (24.7%), reverse dipping (15.6%) and extreme dipping (3.9%). Conclusion a high proportion had nocturnal hypertension (79.2%) and non-dipping pattern was the most prevalent pattern (55.8%). Mean awake systolic BP, mean asleep systolic and diastolic BP and mean 24-h systolic and diastolic BP were elevated. The use of 24-h ABPM will enhance assessment of increased cardiovascular risk and management of Nigerians with hypertension.
BackgroundMixed connective tissue disease (MCTD; also known as Sharp’s syndrome) is a rare autoimmune inflammatory disorder characterized by high titer of U1 ribonucleoprotein (U1RNP) antibody and clinical and serological overlap of systemic lupus erythematosus, systemic sclerosis, and polymyositis. The diagnosis is based on clinical and serological factors in criteria such as Alarcon-Segovia, Khan, Kusakawa, and Sharps. Cardiac disease can be a complication of connective tissue disease (CTD). There are few reports in Africa.AimsTo present MCTD as underlying cause of heart failure with reduced ejection fraction and highlight challenges of investigations and treatment.ObjectivesTo highlight the first case in our center and discuss the cardiac, respiratory, and rheumatologic management.Patient and methodsWe present a 52-year-old woman with 3 weeks history of productive cough with whitish sputum, severe dyspnea, orthopnea, paroxysmal nocturnal dyspnea, right sided abdominal pain, leg swellings, a one year history of recurrent fever, Raynaud’s phenomenon, small joint swellings and deformities with pain in both hands.ResultsOn examination there was microstomia, tethered forehead and lower eyelid skin, tender swelling of the interphalangeal joints and arthritis mutilans. Laboratory findings showed estimated glomerular filtration rate <60 mL/kg/min/1.73 m2, U1RNP antibody levels were eight times upper limit of normal, elevated rheumatoid factor, speckled antinuclear antibody pattern, negative anticentromere antibody, anti Scl-70 and anticyclic citrullinated peptide. Chest X-ray/CT revealed pulmonary fibrosis. Echocardiography findings showed reduced ejection fraction of 40%, elevated pulmonary arterial pressure at rest of 60.16 mmHg. The patient showed improvement on antifailure drugs, but prednisolone was stopped for sudden reversal of previously controlled stage 2 hypertension (HTN), and the patient was discharged in a stable condition. Difficulties ensued in obtaining prompt definite results due to the unavailability of serologic tests in the hospital, and the tests were done outside the state and country.ConclusionIdentifying MCTD is critical, especially in patients requiring steroids that may worsen systemic HTN and heart failure. There is a need to have definitive investigative facilities for such patients in hospitals.
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