Which one of the following antihypertensive medications might you use to try and prevent new-onset atrial fibrillation?
The Losartan Intervention for End Point Reduction in Hypertension (LIFE) study demonstrated a relative risk reduction of 33% versus atenolol. The impact of new-onset diabetes mellitus on cardiac outcomes in the Valsartan Antihypertensive Long-Term Use Evaluation (VALUE) trial population, showed a relative risk reduction of 23% versus amlodopine.
The following is true of hypertension in the elderly, except:
SBP increases with age whereas DBP plateaus at about age 60 resulting in an increased pulse pressure. The elderly have increased variability in their BP, and so several measurements should be made before diagnosis. Beta-blockers should be used in specific circumstances, such as with associated heart failure or CHD, as thiazide diuretics and ACE inhibitors have been shown to be more effective. The Hypertension in the Very Elderly Trial (HYVET) compared indapamide and perindopril treatment versus placebo for patients over the age of 80 with a SBP >160 mmHg. The treatment group had a significant reduction in stroke, mortality (stroke, cardiovascular, and all-cause), and heart failure.
The following are risk factors for pre-eclampsia, except:
Pre-eclampsia is hypertension in pregnancy associated with proteinuria. The blood pressure after 20 weeks is >140/90 mmHg, or a 30/15 mmHg increase from baseline, with 300 mg proteinuria in 24 hours. A new partner is one risk factor for the development of pre-eclampsia, which is believed to be secondary to the immunological basis of the illness. Other risk factors include idiopathic hypertension, obesity, chronic renal disease, and diabetes
Guidelines for the use of a statin in hypertension include the following, except:
Statins should be used in all cases of secondary prevention in patients with hypertension, with target levels of LDL <2 mmol/L and total cholesterol <4 mmol/L or a 30% reduction. The primary prevention benefit of statins has been shown in trials of hypertensive patients down to a CVD risk level of 6%. This is not financially feasible; therefore the recommendation is for statin use if the CVD risk is ≥20% or established type 2 diabetes for more than 10 years. There is little evidence for the treatment of patients over 80 years old with statins.
A 78-year-old woman is referred to cardiology clinic for management of aortic regurgitation. The patient has no cardiac risk factors except mild hypertension (HTN) on monotherapy and has not previously undergone cardiac testing. A review of systems is notable for recent onset of headaches and myalgias.
Physical Examination:
Blood pressure (BP)—138/78 mmHg in both arms; pulse—62 bpm. Funduscopic examination reveals no changes consistent with hypertensive retinopathy. The heart examination is notable for a normal S1 and increased intensity S2 (A2 ). An S4 gallop, II/VI diastolic decrescendo murmur heard best at the right sternal border, and III/VI early-peaking systolic ejection murmur heard at the left sternal border are present. There is no systolic ejection click. The carotid pulse is of normal intensity and contour and the pulses in the upper and lower extremities are strong and equal.
Electrocardiogram (ECG) reveals sinus rhythm with nonspecific ST changes.
What is the most likely explanation for the patient’s heart murmur?
Aortic dilatation with moderate aortic regurgitation and mild aortic stenosis. A bicuspid aortic valve is not likely in a 78-year-old with an initial presentation of aortic valve disease. An aortic ejection click is often present in patients with bicuspid aortic valve disease when the valve is still pliable and is not heard in this patient. Furthermore, the examination is not consistent with severe aortic regurgitation because the diastolic BP is normal (not reduced), the S1 sound is normal in intensity (not reduced as a result of premature closure of the mitral valve), and the carotid pulsations are normal (not bisferiens). The examination is not consistent with severe aortic stenosis because the murmur is early peaking and S2 (A2 ) is audible and not reduced in intensity. The intensity of a systolic ejection murmur is related in part to the stroke volume and not a good single indicator of severity of stenosis. Therefore, the most likely explanation for the heart murmur is aortic dilatation with nonsevere aortic regurgitation and stenosis. Of note, aortic regurgitant murmurs originating from aortic abnormalities are generally heard best along the right sternal border and those originating from valvular disease heard best along the left sternal border.