Diastolic Dysfunction Heart Failure, Diagnostics, and Treatment

Diastolic cardiac insufficiency exists when signs and symptoms of heart failure are present, but the left ventricular systolic function is still preserved (ejection fraction above 45%). It is important to differentiate the diastolic from the systolic heart failure so that it can be optimally treated.

The incidence of diastolic heart failure increases with age; in about 50 percent of elderly patients with heart failure, there is isolated diastolic dysfunction, write Chhabi Satpathy and colleagues in the American Family Physician. If diastolic dysfunction is diagnosed early and adequately treated, the prognosis is better than for systolic dysfunction.

Diastolic heart failure is clinically and radiologically indistinguishable from systolic heart failure. However, if there is a normal ejection fraction and an abnormal diastolic function with signs and symptoms of heart failure, diastolic heart failure can be diagnosed. Unlike systolic, diastolic heart failure can occur in isolation. Common causes of diastolic dysfunction include cardiac ischemia, hypertension, aging, obesity and aortic stenosis. Rarely, the disorder is caused by myocardial diseases such as cardiomyopathy, storage diseases and amyloidosis or sarcoidosis or by a disease of the pericardium.

In isolated diastolic dysfunction, there is a disorder of isovolumic ventricular relaxation and decreased compliance of the left ventricle. The transmission of higher end-diastolic pressures into the pulmonary circulation can cause pulmonary congestion leading to dyspnea and eventually right heart failure.

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Diagnostics

Heart failure may be manifested by fatigue, exertional dyspnoea, paroxysmal nocturnal dyspnea, orthopnea, cervical venous stasis, rales, tachycardia, third or fourth heart sounds, hepatomegaly, and edema. Cardiomegaly and congestion of the pulmonary veins often occur in chest radiographs, but these findings are non-specific and can also occur in non-cardiac diseases. It is difficult to distinguish diastolic from systolic heart failure on the basis of physical examination alone.

Two-dimensional Doppler echocardiography is of great importance in the diagnosis of diastolic heart failure. This study not only provides important information about ventricular size, myocardium, heart valves, systolic function and pericardium, but also provides information on diastolic transmitral and pulmonary venous blood flow. In echocardiography, the peak velocity of blood flow through the mitral valve in the early diastolic filling phase corresponds to the e-wave. The atrial contraction corresponds to the A-wave. From these values, the I / O quotient is calculated. Usually E is greater than A, and the I / O ratio is about 1.5.

In early diastolic dysfunction, relaxation is disturbed and the I / O ratio drops to less than 1.0 with atrial contraction. As the disease progresses, left ventricular compliance decreases, increasing left atrial pressure and early left ventricular filling despite disturbed relaxation. This paradoxical normalization of the I / O quotient is called “pseudo-normalization”. In patients with severe diastolic dysfunction, the left ventricle is filled, especially in early diastole, resulting in an I / O ratio above 2.0. Although cardiac catheterization is preferred in the diagnosis of diastolic dysfunction. However, two-dimensional Doppler echocardiography has proven to be the best noninvasive method in everyday clinical practice. Rarely, radionuclide angiography is performed, especially in patients who find echocardiography technically difficult.

Treatment

Primary prevention of diastolic heart failure includes nicotine abstinence and the aggressive treatment of high blood pressure, hypercholesterolemia and coronary heart disease. Lifestyle changes such as weight loss, cessation of smoking, diet change, restriction of alcohol intake and physical activity serve to prevent diastolic and systolic heart failure. Diastolic dysfunction can remain asymptomatic for many years. Early diagnosis and treatment are important to prevent irreversible structural changes and systolic dysfunction. At first glance, it seems that the treatment of diastolic and systolic heart failure is not very different. However, the treatment of diastolic heart failure is limited due to the lack of large randomized controlled trials. In addition, optimal treatment for systolic heart failure may result in exacerbation of diastolic heart failure.

Improvement of the left ventricular function

For diastolic dysfunction, it is important to control the heart rate and prevent tachycardia to maximize the diastolic filling period. Beta-blockers are particularly useful for this purpose, but they do not directly affect myocardial relaxation. Beta blockers should be used in particular for the treatment of diastolic heart failure, if a high blood pressure, coronary heart disease or arrhythmia.

Optimization of hemodynamics

Hemodynamic optimization is achieved primarily by reducing cardiac preload and afterload. ACE inhibitors and angiotensin receptor blockers directly affect myocardial relaxation and compliance by inhibiting the formation of angiotensin II or blocking angiotensin II receptors, thus preventing interstitial collagen deposition and fibrosis. A Hemodynamic optimization also results in better filling of the left ventricle. and lowering blood pressure. In addition, there is an improvement in exercise capacity and quality of life.

Diuretics may provide optimal intravascular volume in diastolic dysfunction patients, minimize dyspnoea, and prevent acute heart failure. Although diuretics control blood pressure, lead to regression of left ventricular hypertrophy and reduce left ventricular stiffness, some patients with diastolic heart failure are sensitive to preload and develop hypotension or severe prerenal azotemia.

The hormone aldosterone promotes cardiac fibrosis. The aldosterone antagonist spironolactone (Aldactone® or generic) has been studied in a large clinical trial in patients with systolic heart failure. There has been a reduction in heart failure-associated mortality, but the specific effects of spironolactone on diastolic dysfunction are unclear.

Calcium antagonists directly improve diastolic function through myocardial relaxation and indirectly by lowering blood pressure and heart rate, reducing myocardial ischemia, and promoting regression of left ventricular hypertrophy. However, non-dihydropyridine-type calcium antagonists such as verapamil (Isoptin® or generics) and diltiazem (Dilzem® or generic) should not be used in patients with left ventricular dysfunction. Long-acting dihydropyridines such as amlodipine (Norvasc® or generic) should only be used to control heart rate and angina pectoris, If beta blockers are contraindicated or ineffective.

Vasodilators such as nitrates and hydralazine may be useful because of their anti-ischemic and preloading effects, especially if ACE inhibitors can not be used. However, vasodilators should be used with caution as a reduction in preload may reduce cardiac output.

Hypertension and Smoking Addiction – Risks and Dangers

A vicious circle – the best way to describe the interaction of blood pressure with nicotine. At the end of the cycle, in addition to numerous organ diseases, there is also a heart attack. Although the summary of the problem can be expressed very simply, the actual process is highly complex. In addition, smoking addiction can also act as an enhancer of existing blood pressure problems.

The interaction of the organs

The causes of the rise in blood pressure caused by smoking are three main factors. Specifically, they would be bad enough in and of themselves, but their inevitable interaction within body mechanisms makes them even more of a threat.

Sympathetic activity: The sympathetic nervous system is that part of the autonomic nervous system that controls the regulation of blood pressure as well as metabolic and respiratory functions. Under the influence of nicotine, however, this control mechanism gets out of balance and among other things causes an increase in heart activity and resistance within the blood vessels. The result is cardiac arrhythmia and partial to complete occlusion of the vessels.

Vessel constriction: As a result of imbalance in the sympathetic or as a direct effect of smoking addiction, the narrowing of the blood vessels forms the core aspect of nicotine-related hypertension. Responsible for the vascular closure is not only the nicotine per se. Also contained in cigarette smoke additives may favor the arterial closure. Furthermore, the circulation and pumping capacity of the heart and blood vessels are severely impaired by the harmful substances, which offers hypertension further bases for manifestation. In this context, the danger of blood thickening caused by the smoke should not be underestimated, which may lead to further blockage of the vessels.

Lack of oxygen: Since the cigarette smoke a large amount of carbon monoxide gets into the blood, with permanent nicotine consumption and the supply of organs, especially the heart, with oxygen at risk. Now O2 is of essential importance for the integrity of the organs and their functionality. A deficiency supply therefore brings about serious organ damage. Heart attacks and strokes are thus the worst danger when smoking, while hypertension in this area, merely ‘a precursor to the complete failure of the heart.

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The interaction of risk factors

The exact value of systolic blood pressure increase is between 7 mmHg and 10 mmHg when smoking. However, further increases may be added if smoking is associated with one of the following aspects.

    • Smoking due to stress in most cases implies that high blood pressure is already present before consumption. This results from the increased heart activity that results from stressful situations.
    • The same applies to cigarette consumption in combination with obesity. In addition, weight-related arteriosclerosis and vasoconstrictive substances meet and, together, provide even greater resistance within the blood vessels.
    • Smoking addiction in concert with alcohol can not only increase the risk of hypertension, but also of cardiac arrhythmia. As nicotine constricts the vessels, alcohol temporarily expands them so that the pumping intervals of the heart become completely out of balance.

Also in connection with lack of exercise or a wrong diet, the risk of high blood pressure by smoking is greater than normal. In addition to the dysfunctional properties of nicotine here are still added to nutrient deficiency or resilience problems that affect the activity of the heart and organs. Already existing dysfunctions of the organs, such as those caused by unhealthy foods or too little exercise, are further expanded by smoking cigarettes.