**2.4 The treatment of DHF**

Almost randomized, double-blind studies of therapy for HF are studies of systolic dysfunction. Guidelines for the management of patients with chronic HF have been published by several organizations. The management of patients with DHF is not different from that of HF patients with a reduced EF. They include daily monitoring of weight, attention to patient education, and close medical follow-up. The role of cardiac rehabilitation in patients with DHF has also been explored.[23]

The treatment of diastolic heart failure can be demonstrated the following 3 strategies. First, treatment should target symptom reduction by decreasing pulmonary venous pressure at rest and during exertion. Second, treatment should target the pathological disease that caused the diastolic heart failure. For example, coronary artery disease, hypertensive heart disease and diabetes mellitus provide relatively specific therapeutic targets, such as lowering of blood pressure, induction of hypertrophy regression, blood sugar control and treatment of ischemia by increasing myocardial blood flow and reducing myocardial oxygen demand. Third, treatment should target the underlying mechanisms that are altered by the disease processes.

Diuretics are advised for therapy of diastolic HF in the ACC/AHA Guidelines for Evaluation and Management of Heart Failure. The use of diuretics may improve breathlessness in patients with diastolic HF, because circulating blood volume is a major

Although HF preserved EF has been thought to occur primarily inpatients with LVH, studies that have carefully quantified LV mass report that echocardiographic criteria for

Increases in the left atrial dimension or volume are commonly present in patients with HF

Just as chronic pulmonary venous hypertension leads to pulmonary arterial hypertension in HF with reduced EF, the same can occur in HF preserved EF, and an elevated tricuspid regurgitant velocity indicative of pulmonary hypertension is extremely common in HF

Regional wall motion abnormalities with preserved EF and right ventricular dilatation, either from ischemic disease or secondary to chronic pressure overload from chronic pulmonary venous hypertension, can also be present at echocardiography in patients with HF preserved EF. Additional negative findings at echocardiography include the absence of valvular disease, pericardial tamponade, pericardial constriction, the presence of congenital heart diseases such as atrial septal defect, other more extensive structural abnormalities are

Almost randomized, double-blind studies of therapy for HF are studies of systolic dysfunction. Guidelines for the management of patients with chronic HF have been published by several organizations. The management of patients with DHF is not different from that of HF patients with a reduced EF. They include daily monitoring of weight, attention to patient education, and close medical follow-up. The role of cardiac

The treatment of diastolic heart failure can be demonstrated the following 3 strategies. First, treatment should target symptom reduction by decreasing pulmonary venous pressure at rest and during exertion. Second, treatment should target the pathological disease that caused the diastolic heart failure. For example, coronary artery disease, hypertensive heart disease and diabetes mellitus provide relatively specific therapeutic targets, such as lowering of blood pressure, induction of hypertrophy regression, blood sugar control and treatment of ischemia by increasing myocardial blood flow and reducing myocardial oxygen demand. Third, treatment should target the underlying mechanisms that are altered by the

Diuretics are advised for therapy of diastolic HF in the ACC/AHA Guidelines for Evaluation and Management of Heart Failure. The use of diuretics may improve breathlessness in patients with diastolic HF, because circulating blood volume is a major

LVH are met in less than 50% of patients. [15-18]

**2.3.4 Pulmonary hypertension in diastolic heart failure** 

**2.3.5 Other echocardiographic findings in diastolic heart failure** 

rehabilitation in patients with DHF has also been explored.[23]

**2.3.3 Left atrium in diastolic heart failure** 

important enough to cause the HF symptoms.

preserved EF. [19-21]

preserved EF.[19, 22]

**2.4 The treatment of DHF** 

disease processes.

determinant of ventricular filling pressure. In spite of chronic data are lacking on nitrates, they are effective on the diastolic HF in the acute phase, because of deceasing central blood volume by vasodilating. In spite of chronic data are also lacking on human atrial natriuretic peptides, they are effective on the diastolic HF in the acute phase, because of deceasing central blood volume by natriuretic and vasodilating effect. Digoxin was reported to yield symptomatic improvement and decreased hospitalizations without mortality benefit in the DIG study in patients with DHF.[24]

We treat with angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) and aldosterone antagonists in the chronic systolic heart failure patients, because the rennin-angiotensin- aldosterone system (RAAS) plays the pivotal roles on the left ventricular remodeling in HF patients.[25] Recent studies of HF patients with preserved LV function suggest that ACE inhibitors or ARBs may improve functional class, exercise duration, ejection fraction, diastolic filling and LV hypertrophy. In the large randomized trial of perindopril (an ACE inhibitor) for patients older than 70 years with chronic HF and normal or near-normal EF, event rates were lower than anticipated. Some trends toward benefit, primarily driven by reduction in HF-related hospitalizations, were observed at 1 year (PEP-CHF trial).[26] In the CHARM-Preserved Trial, [27] HF patients with an EF higher than 40% were randomized to candesartan ( an angiotensin receptor antagonist ) or placebo in addition to standard therapy. Fewer patients in the candesartan group than in the placebo group reached the primary endpoint of cardiovascular death or HF hospitalization, a finding that reached statistical significance only after adjustment for nonsignificant differences in baseline characteristics. Then, irbesartan (an ARB) did not improve the outcomes of DHF patients (I-PRESERVE).[28] Although candesartan and irbesartan are angiotensin receptor blockers, the results of the trials are different. These pleiotropic effects may be different. The trial of aldosterone antagonists for DHF patients is going on in DHF patients (TOPCAT trial). Beta blocker has been shown to improve morbidity with diastolic and systolic HF. [29,30] Although calcium channel antagonists can improve measures of diastolic function during short-term use, definitive data with chronic administration for diastolic HF are not available. Recent reports show statins reduce the number of cardiovascular hospitalizations in patients with systolic heart failure, although they did not reduce the primary outcome which is the composite of death from cardiovascular causes, non fatal myocardial infarction and nonfatal stroke.[31,32] A few trials of statins have shown to improve the mortality in patients with DHF [33]. Further investigations are needed.
