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CHAPTER 9

Management of Complicated hypertension
Coronary Artery Disease
  • The level of blood pressure is continuously related to the risk of coronary artery disease.
  • Hypertensive patients, particularly in the presence of left ventricular hypertrophy may present with angina pectoris without angiographic evidence of epicardial coronary artery disease.
  • Exercise ECG and stress myocardial perfusion imaging occasionally yield false positive results in hypertensive patients.
  • B-blockers are the drugs of choice for hypertension in patients with coronary artery disease. Calcium antagonists offer a good alternative for patients who cannot tolerate B-blockers. ACE-inhibitors are extremely useful in the presence of left ventricular dysfunction.
  • Aspirin, statins and ACE inhibitors may reduce the risk of future cardiovascular events.
  • Caution should be taken when aggressively lowering blood pressure in hypertensive patients with left ventricular hypertrophy and coronary artery disease.

Relation of Blood Pressure to Coronary Artery Disease

  • There is a continuous and graded relationship between blood pressure and risk for coronary artery disease. Lowering blood pressure can reduce this risk.
  • Patients with coronary artery disease and hypertension are at particularly high risk for cardiovascular morbidity and mortality. The benefits and safety of antihypertensive therapy in such patients are well established.
  • Concerns have been raised that lowering diastolic blood pressure too much may increase the risk of coronary events by lowering diastolic perfusion pressure in the coronary circulation. The hypertension optimal treatment trial (HOT) has revealed that the optimal diastolic blood pressure level corresponding to minimal risk is approximately 83mmHg. Below this level there is little apparent further benefit in terms of reducing the number of major cardiovascular events.

Diagnosis of Coronary Artery Disease in Hypertensive Patients

  • Some patients with hypertension, especially if associated with left ventricular hypertrophy, may have angina, positive exercise ECG, or perfusion defects in stress myocardial imaging without angiographic evidence of coronary artery disease.
  • Stress echocardiography (most frequently with dobutamine) is more specific than exercise ECG or stress myocardial perfusion imaging.
  • Coronary angiography is indicated when the results of non-invasive tests are inconclusive.

Management of Hypertension in Patients with Coronary artery Disease

Hypertensive patients with stable angina

  • Beta-blockers may be specifically useful in patients with hypertension and stable angina.
  • Calcium antagonists offer a good alternative therapy when beta-blockers are contraindicated or ineffective. Short-acting calcium antagonists should not be used.

Hypertensive patients with acute coronary syndromes

  • The appropriate initial treatment of severe hypertension should include IV nitrates.
  • Beta-blockers may be valuable when the blood pressure is moderately raised.
  • Sodium nitroprusside should be reserved for resistant cases, as it may exacerbates coronary ischemia.
  • An ACE inhibitor may be administered when hypertension persists despite treatment with nitroglycerin and a beta blocker. It should be given as early as possible in patients with LV systolic dysfunction or congestive heart failure or large myocardial infarction.
  • When beta blockers are contraindicated, a non-dihydropyridine calcium antagonist (e.g., verapamil or diltiazem) is recommended.
  • Immediate release dihydropyridine calcium antagonists should be avoided in the absence of a beta blocker.

Hypertension in the post-myocardial infarction patient

  • Hypertension should be controlled to a blood pressure of 130/85 mmHg.
  • Unless contraindicated, beta blockers should be used following a myocardial infarction. Beta blockers have been shown to reduce the risks of both reinfarction and cardiovascular death by about 25 %. 
  • ACE inhibitors are recommended after myocardial infarction especially in patients with left ventricular dysfunction or heart failure since they reduce by about one-fifth the risk of myocardial infarction or sudden death. They also retard the process of myocardial remodeling and may prevent progression of heart failure.
  • There is no clear evidence from clinical trials that calcium antagonists (verapamil or diltiazem) reduce recurrent coronary heart disease events.
  • Calcium antagonists (verapamil, diltiazem) may be used if beta blockers are ineffective or contra-indicated. In presence of left ventricular systolic dysfunction, they should better be avoided.

Prevention of coronary artery disease beyond blood pressure control

Since the aim of treatment of hypertension is the reduction in total cardiovascular risk, it is relevant as well to treat other cardiovascular risk factors and associated clinical conditions present in the hypertensive patient.

Anti-platelet Agents

In patients with well-controlled blood pressure, low dose (75 mg) aspirin may be used to reduce the risk of acute myocardial infarction without increasing the risk of cerebral bleeding. In the HOT study, a small dose (75 mg) of aspirin in addition to the antihypertensive treatment significantly reduced the number of major cardiovascular events and all myocardial infarctions compared with placebo.

Cholesterol Lowering Therapy:

The results of several controlled trials have shown that statins treatment reduces the risks of initial and recurrent coronary heart disease events among patients with a wide range of initial cholesterol levels. Statin treatment also reduces the risk of stroke substantially in patients with coronary heart disease. The benefits were similar in hypertensive patients. Statins are recommended for hypertensive patients with hyperlipidemia and for those at increased risk of coronary heart disease.

Angiotensin Converting Enzyme Inhibitors:

The heart outcome prevention evaluation study (HOPE) was carried out in high-risk patients who received ramipril (10 mg/day). Ramipril-treated patients experienced a 22 percent reduction in the composite endpoint, which resulted in a reduction in the risk of death from any cause. This effect appears largely independent of the ACE inhibitors blood pressure lowering effects. The benefits derived from ACE inhibitors are presumed to be primarily due to a direct protective mechanism upon the vascular wall, possibly by improving endothelial function and reducing plaque activation.

 

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