As early as 1881, Mayer described a clinical picture that included heart failure as a "frequent and remarkable complication of diabetes mellitus" (Stratmann 2018).
The term diabetic cardiomyopathy was first coined by Rubler et al. in 1972 (Stratmann 2018) as a "myocardial dysfunction in patients with diabetes in the absence of coronary artery disease, hypertrophy, or valvular disease" (Marx 2019).
According to the WHO, cardiomyopathy is defined as a disease of the myocardium that is associated with cardiac dysfunction (Erdmann 2009) or a disease of the myocardium that is causally caused by diabetes mellitus and occurs independently of CHD or arterial hypertension (Stratmann 2008). It can lead to both systolic and diastolic dysfunction (Haag 2012).
To date, however, it is unclear whether or not diabetic cardiomyopathy exists as a separate disease entity (Marx 2019). On the other hand, it represents one of the most frequent and most dangerous complications or concomitant diseases of diabetes mellitus (Stiefelhagen 2015).
According to the American Heart Association, diabetic cardiomyopathy is a secondary cardiomyopathy (Erdmann 2009).
According to the WHO classification of cardiomyopathies, a distinction is made between:
Cardiomyopathy leads to chronic heart failure, which is differentiated between:
Diabetic cardiomyopathy occurs predominantly in type 2 diabetics, but has also been diagnosed in long-term type 1 diabetics (Mehnert 2003).
Patients with type 2 diabetes are 4 times more likely to suffer from heart failure than healthy peers. Conversely, approximately 24% of patients with heart failure suffer from a diabetic metabolic condition, and of hospitalized patients, this figure is as high as 40% (Stratmann 2014).
Patients with precursors of diabetes mellitus - such as metabolic syndrome - also have a significantly increased risk of heart failure. But conversely, patients with non-ischemic cardiomyopathy are more likely than the general population to develop diabetes mellitus and/or insulin resistance later in life (Stratmann 2014).
8 - 15 years after diagnosis, the risk of suffering a myocardial infarction is just as high for diabetics - without recognizable macrovascular diseases - as it is for non-diabetics after myocardial infarction (Mehnert 2003).
The cause of diabetic cardiomyopathy is diabetes mellitus disease.
Risk factors for the development of heart failure in diabetics are:
The pathophysiological relationships have not yet been sufficiently clarified. It is assumed that hyperglycemia, hyperlipidemia and hyperinsulinemia lead to changes in myocardial metabolism, which in turn cause functional and structural disorders (Stratmann 2014).
Activation of the renin-angiotensin system, impaired calcium homeostasis, increased oxidative stress, mitochondrial dysfunction and impaired substrate metabolism are thought to play a role (Haag2012).
Cellular effects result in:
This causes an energy deficiency situation for the heart muscle despite energetic oversupply (Stratmann 2014).
Diabetic cardiomyopathy manifests in different areas:
This manifests itself in ventricular dysfunction similar to dilated cardiomyopathy, with increased left ventricular volume, reduced stroke volume and left ventricular hypokinesia. Diastolic dysfunction usually precedes systolic dysfunction.
This is also known as "autonomic neuropathy". It affects both sympathetic and parasympathetic innervation, with vagal efferents being affected much earlier and to a greater extent.
It is also called "diabetic microangiopathy". Under stress, insufficient glucose and lactate are available to the myocardium due to insulin receptor and glucose transporter defects.
Degenerative changes in the vascular system occur as a result of vasculopathy. These are not necessarily caused by hyperlipidemia, as was still assumed until the 1970s (no atherosclerosis of the large vessels was detectable angiographically and autoptically in 30%-50%).
(Gerok 2007)
Not infrequently, early stages of the disease are asymptomatic.
The clinical picture otherwise corresponds to that of other cardiomyopathies:
(Erdmann 2009)
Even in non-symptomatic patients, tissue Doppler echocardiography should be performed as screening (Stratmann 2014).
On physical examination may be present:
(Gerok 2007)
(Erdmann 2009). This is often an early marker of disease (Marx 2019).
Tissue Doppler echocardiography.
Tissue Doppler has particular value in the diagnosis of early heart failure.
The determination of BPN may have a value in asymptomatic diabetics for the detection of left ventricular dysfunction and also with regard to prognosis, as shown in a study by Bhalla et al. (2004) (Tschöpe 2006).
(Stratmann 2008)
(Erdmann 2009)
(Tschöpe 2006)
(Erdmann 2009)
There is a significantly increased mortality after myocardial infarction and in the presence of heart failure. Diabetic cardiomyopathy is considered to be the cause (Tschöpe 2006).
The therapy corresponds to the treatment of other cardiomyopathies (Marx 2019), such as with ACE inhibitors, AT1 receptor antagonists or beta receptor blockers (Tschöpe 2006).
Specific recommendations for diabetic cardiomyopathy cannot be given due to the lack of prospective studies.
For diabetic patients with heart failure, two insurance databases have found reduced mortality in patients treated with metformin. However, metformin is problematic in symptomatic patients because of the risk of lactic acidosis.
A reduced mortality was also found with glitazone therapy. However, glitazone may adversely affect pre-existing heart failure due to fluid retention.
(Erdmann 2009)
For heart failure with preserved left ventricular function (HFpEF), which is present in up to 50% of diabetic patients, only symptomatic therapy exists to date (Marx 2019).
A recently published study shows a rapid and highly significant reduction in hospitalization for heart failure with treatment with SGLT2- inhibitors such as dapagliflozin or empagliflozin (Marx 2019).
Dosage recommendation: dapagliflozin 10 mg 1 x / d, empagliflozin 25 mg 1 x / d (Müller 2021).
Of great importance, in addition to the adjustment of blood sugar, is that of blood pressure. Here, the lowest tolerable adjustment of blood pressure with diuretics, ACE inhibitors, AT1 receptor antagonists or beta receptor blockers should be aimed for (Tschöpe 2006).
Since glitazones can cause fluid retention with peripheral edema, they are considered contraindicated in diabetic cardiomyopathy. Treatment with metformin should be avoided from NYHA III onwards (Tschöpe2006).
Nearly all mortality in diabetics is cardiovascular (Just 2013).
There is evidence that diabetes-related cardiomyopathy can be alleviated by insulin therapy (Kasper 2015).
Diabetics who have heart failure have a 5-year survival rate of only 12% (Herold 2020). Diabetics with decompensated heart failure have an even worse prognosis. After 6 months, > 20 % have already died (Tschöpe 2006).
The cardiovascular death rate in male patients with diabetes mellitus is increased twofold and fourfold in women (Kasper 2015).
Patients with diabetic cardiomyopathy are comparatively more likely to develop pulmonary edema, cardiogenic shock, and left heart failure after infarction. The death rate after infarction is also significantly increased compared to patients without an additional diabetes mellitus disease (Mehnert 2003).