AHA guidelines for controlling hypertension in ACS patients
General Principles Of BP Management In The Patient With ACS Patients with ACS are especially vulnerable to an alteration in the supply demand equation such that ischemia occurs at rest or at relatively low levels of demand. Although an elevated BP increases myocardial oxygen demand, rapid and excessive lowering of the DBP has the potential to result in impairment of coronary blood flow...
Patients with ACS are especially vulnerable to an alteration in the supply demand equation such that ischemia occurs at rest or at relatively low levels of demand. Although an elevated BP increases myocardial oxygen demand, rapid and excessive lowering of the DBP has the potential to result in impairment of coronary blood flow and oxygen supply.
In addition, patients with ACS often have vasomotor instability with an increased tendency to exaggerated responses to antihypertensive therapy.
The selection of antihypertensive agents for use in the patient with ACS should be focused on selecting drugs that have an established evidence-base for risk reduction for patients with ACS independently of BP lowering. These drugs, which include b-blockers, ACE inhibitors (or ARBs), and, in selected patients, aldosterone antagonists, should typically be titrated to full doses before other agents that do not have an established evidence base are initiated.
AHA had come with new guidelines in the year 2015, which redefined the goals as well the strategy of management of hypertension in patients with Acute Coronary Syndrome. Here is a summary of those goals and strategies
Therapeutic targets for BP have not been established specifically for patients with ACS. Current guidelines recommend a BP target of< 140/90 mm Hg and <130/80 mm Hg for patients with diabetes mellitus or CKD (1,187), but this applies more to secondary prevention than the management of hypertension in the acute phase of MI. The BP may fluctuate early after ACS; thus, efforts should focus on pain control and clinical stabilization before BP is specifically targeted. Second, the BP should be lowered slowly, and caution is advised to avoid decreases in DBP to < 130/80 mm Hg at the time of hospital discharge is a reasonable option.
In older hypertensive individuals with wide pulse pressures, lowering SBP may lead to very low DBP values, contributing to worsening myocardial ischemia.
If there is no contraindication to the use of b-blockers, in patients with ACS, the initial therapy of hypertension should include a short-acting b1-selective b-blocker without intrinsic sympathomimetic activity (metoprolol tartrate or bisoprolol).
b-Blocker therapy should typically be initiated orally within 24 hours of presentation (Class I; Level of Evidence: A). For patients with severe hypertension or ongoing ischemia, an intravenous b-blocker (esmolol) can be considered (Class IIa; Level of Evidence: B).
For hemodynamically unstable patients or when decompensated HF exists, the initiation of b-blocker therapy should be delayed until stabilization has been achieved (Class I; Level of Evidence: A).
In patients with ACS and hypertension, nitrates should be considered to lower BP or to relieve ongoing ischemia or pulmonary congestion (Class I; Level of Evidence: C). Nitrates should be avoided in patients with suspected right ventricular infarction and in those with hemodynamic instability.
Sublingual or intravenous nitroglycerin is preferred for initial therapy and can be transitioned later to a longer-acting preparation if indicated.
If there is a contraindication to the use of a b-blocker or intolerable side effects, then a nondihydropyridine CCB such as verapamil or diltiazem may be substituted for patients with ongoing ischemia, provided that LV dysfunction or HF is not present. If the angina or hypertension is not controlled on a b-blocker alone, a longer-acting dihydropyridine CCB may be added after optimal use of an ACE inhibitor (Class IIa; Level of Evidence: B).
An ACE inhibitor (Class I; Level of Evidence: A) or an ARB (Class I; Level of Evidence: B) should be added if the patient has an anterior MI, if hypertension persists, if the patient has evidence of LV dysfunction or HF, or if the patient has diabetes mellitus
For lower risk ACS patients with preserved LV ejection fraction and no diabetes mellitus, ACE inhibitors can be considered a first-line agent for BP control (Class IIa; Level of Evidence: A).
Aldosterone antagonists are indicated for patients who are already receiving b-blockers and ACE inhibitors after MI and have LV dysfunction and either HF or diabetes mellitus. Serum potassium levels must be monitored.
These agents should be avoided in patients with elevated serum creatinine levels (‡2.5 mg/dL in men, ‡2.0 mg/dL in women) or elevated potassium levels (‡5.0 mEq/L) (Class I; Level of Evidence: A).
Loop diuretics are preferred over thiazide and thiazide-type diuretics for patients with ACS who have HF (NYHA class III or IV) or for patients with CKD and an estimated glomerular filtration rate < 30 mL/min.
For patients with persistent hypertension not controlled with a b-blocker, an ACE inhibitor, and an aldosterone antagonist, a thiazide or thiazide-type diuretic may be added in selected patients for BP control (Class I; Level of Evidence: B).
Dr. Manav Aggarwal is a Interventional Cardiologist,Cardiologist and General Physician in Darya Ganj, Delhi and has an experience of more than 10 years in these fields. Dr. Manav Aggarwal practices at Sanjeevan Hospital in Darya Ganj, Delhi.