Welcome Letter

Dear Colleagues,
It is our pleasure to invite you to participate in the 7th International Conference on Prehypertension, Hypertension, Metabolic Disorders and Cardiovascular Disease, which will take place in Vilnius, Lithuania from October 15-18, 2020.

The definition of borderline levels of blood pressure, plasma glucose and plasma lipids changed during the last decades. When clustering of these appears, it is not easy to decide about treatment- when it should be initiated and how will be the best way to protect the patient from complications and to prevent development of cardiovascular disease. In principle, therapeutic decisions were made by estimating the patient’s cardiovascular risk. The higher the risk the earlier treatment should be initiated.

It has been shown that clustering of the components of the Cardiometabolic syndrome magnifies significantly the rate of progression of both atherosclerosis and arteriosclerosis, leading to overt damage in the heart, brain, kidneys and other organs.

Progression of damage appears gradually in the arteries. It starts as a functional change accompanied at a later stage by structural changes. These changes occur gradually also with the process of aging, but are significantly accentuated by cardiovascular risk factors.

Multiple factors affect the rate of progression of damage, among them- genetic factors, lifestyle, stress, smoking, alcohol intake and others. Interventions like change in life habits and medical treatment to correct all components of the Cardiometabolic syndrome – lowering blood pressure, plasma cholesterol, plasma glucose, treatment of obesity and cessation of smoking and of alcohol intake should be performed in each patient.

Organ specific changes appear and lead to morbidity and mortality. Damage to the heart can include coronary artery disease, cardiac hypertrophy, diastolic dysfunction and leads to IHD, myocardial infarction, heart failure and death. In the brain changes in the large arteries like the carotid artery, supplying blood to the brain and the small arteries, can lead to cerebrovascular ischemia and infarction, which can be embolic or ischemic. The damage can lead to lacunar infarcts, ischemic or hemorrhagic stroke, causing disability and death.

In approaching this wide world problem, we should act to prevent the damage and when already present to stop its progression and even to induce damage regression.

The research in the field needs new diagnostic methods in order to enable early diagnosis before symptom development and new therapeutic approaches, medical and instrumental.

Understanding of yet unknown pathophysiologic aspects of disease development are also needed.

The purpose of our meeting is to discuss in depth new mechanisms of cardiovascular damage development, novel methods of diagnosis and new therapeutic approaches.

Yours sincerely,