Cardiology – 5th Edition

By R. H. Swanton
Published 2003
Blakwell Publishing
Cardiology/ Handbooks, manuals, etc
464 pages
ISBN:1405101970
Cardiology is a rapidly changing and expanding field. Management protocols change regularly, new categories of treatment options are being discovered, and there is a new focus on the prevention of cardiovascular diseases.Pocket Consultant: Cardiology is a highly practical, user-friendly guide to this expanding field. Now in its fifth edition, this book has been highly praised for its readability, conciseness and clear illustrations, and is an indispensable guide for those dealing with common cardiological problems. The author, the current president of the British Cardiac Society, is internationally known in the field of clinical cardiology. This is an ideal book for the junior doctor who wants a quick, easily understandable guide to cardiology.

First Ever Triple Heart Valve Replacement Surgery

At Portneuf Medical Center, it’s the first surgery in the history of the hospital, a successful triple heart valve replacement. Local News 8 introduces you to the recipient of that successful surgery and checks the recovery process.
“It’s great. It turned out so well.” says Sandra Matthews, the triple valve replacement surgery recipient. Sandra Matthews is a young 65-year-old woman from Pocatello and Tuesday she under-went a very risky surgery.
One that is usually performed on a university level but for the first time in the history of the Portneuf Medical Center, a triple heart valve replacement surgery was successfully completed. Doctors expected a double valve replacement, but when they got inside, they found 3 valves had to be replaced. “These are such high risk operations to be able to be done and we can do these operations here in Pocatello.” Says Dr. Jacob DeLaRose, Chief of Cardiac Surgery at Portneuf Medical Center.

Doctors tell Sandra she’s set to head back home in just a few days. But just 24 hours ago she was a little concerned going into surgery but knew her heart was in good hands. “I knew I was going to be out here. I’ve got too much fishing and 4-wheeling and camping to do yet.” Says Matthews.
Doctors at PMC say triple heart valve replacement surgery is one of high risk but one thing helped Sandra get through the extraordinary surgery.
“I’m a firm believer that to have a positive attitude and positive outlook is what gets you through the operation. We’re the technicians but you have to have it inside and in here and you’ll be able to do great.” Says Dr. DeLaRosa. As for Sandra, she already has a game plan after she leaves the hospital. “To get home and see my little dogs that are going crazy because I’m not there.” Says Matthews.
Portneuf Medical Center says future operations of this stature depend on an individual case-by-case basis. Doctors say they hope to perform more in the future.

Ventricular Premature Complexes

Background
Ventricular premature complexes (VPCs) are ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular arrhythmia. Assessment and treatment of VPCs is challenging and complex. The significance of VPCs is interpreted in the context of the underlying cardiac condition.
The approach to the evaluation and management of VPCs has undergone dramatic changes in the last decade. Ventricular ectopy leading to ventricular tachycardia (VT), which, in turn, can degenerate into ventricular fibrillation, is one of the common mechanisms for sudden cardiac death. The treatment paradigm in the 1970s and 1980s was to eliminate VPCs in patients after myocardial infarction (MI). Recent arrhythmia suppression studies have demonstrated that eliminating VPCs with available antiarrhythmic drugs increases the risk of death to patients without providing any measurable benefit.
Pathophysiology
Very few studies have evaluated the pathophysiology of VPCs in human subjects. Most of the information is derived from animal studies. Three common mechanisms exist for VPCs, (1) automaticity, (2) reentry, and (3) triggered activity, as follows:

Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC. In animal models, focal mechanisms without evidence of macro-reentry play a major role in the origin of ventricular arrhythmia associated with ischemic cardiomyopathy. Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium.
Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. The slow-conducting tissue could be due to damaged myocardium, as in the case of a healed MI.
Triggered activity: Afterdepolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a VPC. Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated VPCs, but they also can be present with ischemia and electrolyte abnormalities.
Frequency
United States
The reported prevalence of VPCs varies between studies, depending on the population studied, duration of observation, and method of detection. In asymptomatic patients, VPCs are infrequent when only a single 12-lead ECG is used for screening. The Framingham heart study (with 1-h ambulatory ECG) suggested that the prevalence rate of 1 or more VPCs per hour was 33% in men without coronary artery disease (CAD) and 32% in women without CAD. Among patients with CAD, the prevalence rate of 1 or more VPCs was 58% in men and 49% in women. Other studies using 24-hour ambulatory monitoring showed a VPC prevalence rate of 41% in healthy teenage boys aged 14-16 years, 50-60% in healthy young adults, and 84% in healthy elderly persons aged 73-82 years. VPCs also are common in patients with hypertension, ventricular hypertrophy, cardiomyopathy, and mitral valve prolapse.
International
Data from the Gruppo Italiano per lo Studio della Sopravvivenza dell'Infarto Miocardico 2 study demonstrated that 64% of patients who had MI then had ventricular arrhythmia and 20% of patients had more than 10 VPCs per hour when 24-h Holter monitoring was used.
Mortality/Morbidity
Prognosis depends on the frequency and characteristics of VPCs and on the type and severity of associated structural heart disease. VPCs are associated with an increased risk of death, especially when CAD is diagnosed, but the relationship between VPC frequency and mortality, even in this group, is not robust and no benefit results in suppressing VPCs to improve survival in any population.

In asymptomatic patients, frequent ventricular ectopy (defined as a run of 2 or more consecutive premature ventricular depolarizations or with premature ventricular depolarizations constituting >10% of all ventricular depolarizations on any of the ECG recordings with the subject at rest, during exercise, or during recovery) recorded during exercise testing was associated with 2.5-fold increased risk of cardiovascular death. Less frequent VPCs did not increase the risk.

In general, multimorphic VPCs connote a poorer prognosis than uniform morphologic VPCs. In patients post-MI, frequent VPCs (>10/h) are associated with increased mortality in the prethrombolytic era, but the association in patients receiving thrombolysis is weak.

In a recent study, a frequent VPC (defined as the presence of 7 or more ventricular premature beats per minute during any given stage, ventricular bigeminy, ventricular trigeminy, ventricular couplets, ventricular triplets, sustained or nonsustained ventricular tachycardia, ventricular flutter, torsade de pointes, or ventricular fibrillation) during recovery from exercise was an independent predictor of death. However, frequent VPCs only during exercise did not independently predict an increased risk.

Frequent VPCs, especially when they occur in a bigeminal pattern, can precipitate tachycardia-induced cardiomyopathy that can be reversed by elimination of the PVCs through catheter ablation.
Sex
The Framingham heart study demonstrated increased prevalence of VPCs in men compared with women. The difference was especially higher in men with CAD than in women with CAD.
Age
VPCs are uncommon in children (suggested prevalence rate of 0.8-2.2% from the Vanderbilt Medical Center; exact prevalence not known). Prevalence increases with age.
History
Various symptoms are associated with VPCs, but the exact prevalence of symptoms is not known. Typical symptoms include palpitations, light-headedness, syncope, atypical chest pain, or fatigue. Palpitations are due to an augmented post-VPC beat and may be sensed as a pause rather than an extra beat.
Physical
VPCs frequently are associated with variable or decreased intensity of heart sounds. The augmented beat following a dropped beat is heard frequently. Bounding jugular pulse (cannon A wave) from a loss of atrioventricular (AV) synchrony may be present. The follow-up beat after a VPC is stronger due to the postextrasystolic compensatory pause, allowing greater left ventricular (LV) filling, which usually causes greater intensity of that beat. This is known as extrasystolic potentiation.
Lab Studies
Look for correctable causes of VPCs, such as medications, electrolyte disturbances, infection, and myocardial ischemia or MI.
Obtain serum electrolyte and magnesium levels.
Imaging Studies
Look for underlying structural heart abnormalities that can predispose to VPCs.
·
Assess the degree of LV dysfunction by noninvasive techniques such as echocardiography or radionuclide imaging.
Echocardiography may be preferable because it also provides structural information about the heart.
Other Tests
In high-risk patients, ie, those with reduced ejection fraction (EF) and VPCs, a 24-hour Holter monitor may help establish the degree of electrical instability.
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The severity of LV dysfunction, along with the complexity and frequency of the VPC, determines the aggressiveness of management.
Suppressing the VPCs themselves is not the focus of treatment unless patients are extremely symptomatic; rather, treatment may be implemented if the patient is felt to be at high risk of sudden cardiac death.
Treatment of the underlying structural heart disease also is extremely important. This includes acute syndromes, such as ischemia and infarction, the treatment of which involves reperfusion.
ECG should be performed to look for structural cardiac abnormalities. Diagnostic criteria include the following:
·
Wide (duration exceeding the dominant QRS complexes) and bizarre QRS complexes are present.
No preceding premature P waves occur, and, rarely, a sinus P wave is conducted.
The T wave usually is in the opposite direction from the R wave.
Full compensatory pause is common.
VPCs originating from the left ventricle typically produce a right bundle-branch block (BBB) pattern on QRS.
VPCs originating from right ventricle typically produce left BBB-like pattern on QRS.
Idiopathic VPCs often originate from the right ventricular outflow tract and have a left bundle rightward axis morphology.
Electrophysiologic study
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Electrophysiologic study (EPS) may be indicated for 2 types of patients with VPCs, (1) those with a structurally normal heart with symptomatic VPCs, for whom pharmacological treatment or catheter ablation is indicated and (2) those with VPCs and structural heart disease, for whom risk stratification for sudden cardiac death is indicated.
According to current American College of Cardiology/American Heart Association guidelines, class I indications for EPS are patients with CAD, low EF (<0.36), and nonsustained VT on ambulatory ECG. Class II indications for catheter ablation apply to patients with a highly symptomatic uniform morphology of VPC, couplets, and nonsustained VT.
Exercise stress testing should be performed to look for coronary ischemia, exercise-induced arrhythmia, or both.

Influence of right ventricular pressure overload on left and right ventricular filling in cor pulmonale assessed with Doppler echocardiography.

We evaluated the influence of right ventricular (RV) pressure overload on RV and left ventricular (LV) filling using Doppler echocardiography in cor pulmonale. The LV and RV inflow signals were recorded by Doppler flowmetry. The end-diastolic (ED) and end-systolic (ES) LV short axis images were detected by 2-dimensional echocardiography in 20 healthy subjects and in 36 cases of chronic pulmonary disease (CPD) with pulmonary hypertension. We measured (1) the ratio of the peak velocity of inflow due to atrial contraction to the peak velocity of rapid inflow (A/R), (2) the deceleration half-time of rapid inflow (delta TD), (3) the corrected radius of curvature (cRC) of the interventricular septum (IVS) at ES and ED, and (4) the percent change of length of 16 radial grids (%CL) using the fixed method on the ED and ES short axis images. In 17 of 36 patients with CPD, we measured the systolic pulmonary artery pressure (sPAP), the cardiac index (CI), the mean pulmonary capillary wedge pressure (mPCWP), the end-diastolic right ventricular pressure and the partial oxygen pressure of arterial blood (PaO2). The results were as follows: in CPD, (1) both the RV and the LV diastolic behavior were impaired as shown by increased A/R (1.04 +/- 0.20, 0.98 +/- 0.17, respectively) and prolonged delta TD (115 +/- 20, 100 +/- 17 msec, respectively), (2) the IVS was flattened at ED (cRC of IVS = 0.67 +/- 0.12), (3) the IVS wall motion was impaired (%CL of IVS = 133 +/- 13), (4) the sPAP had an adequate correlation with RV A/R (r = 0.80, p less than 0.01), RV delta TD (r = 0.59, p less than 0.05), LV A/R (r = 0.82, p less than 0.01), LV delta TD (r = 0.61, p less than 0.05), cRC of IVS (r = 0.67, p less than 0.01), %CL of IVS (r = -0.59, p less than 0.05). There was no significant correlation between the LV diastolic behavior and the CI, the mPCWP, the PaO2. It is concluded that the impairment of RV diastolic behavior was caused by the decreased RV compliance due to RV free wall hypertrophy. Moreover, the RV pressure overload interfered with the IVS motion during diastole, this regional impairment of diastolic behavior of the IVS subsequently causing impairment of LV diastolic filling.

Interventricular mechanical asynchrony in pulmonary arterial hypertension

Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular under filling.

OBJECTIVES: The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening.
BACKGROUND: In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening.
METHODS: In 21 PAH patients (mean pulmonary arterial pressure 55 +/- 13 mm Hg and electrocardiogram-QRS width 100 +/- 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T(onset)) and peak time (T(peak)) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law.
RESULTS: The T(onset) was 51 +/- 23 ms, 65 +/- 4 ms, and 52 +/- 22 ms for LV, septum, and RV, respectively. The T(peak) was 293 +/- 58 ms, 267 +/- 22 ms, and 387 +/- 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 +/- 45 ms, coinciding with septal overstretch and RV T(peak). The L-R delay in T(onset) was -1 +/- 16 ms (p = 0.84), and the L-R delay in T(peak) was 94 +/- 41 ms (p < 0.001). The L-R delay in T(peak) was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T(peak) correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05).
CONCLUSIONS: In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.

Mechanical right ventricular dyssynchrony in patients after atrial switch operation for transposition of the great arteries.

Recent data suggest potential benefits of cardiac resynchronization therapy in the management of right ventricular (RV) dysfunction in congenital heart disease. The aim of this study was to determine the nature, prevalence, and functional implications of mechanical RV dyssynchrony in patients after Senning or Mustard procedures for transposition of the great arteries. Twenty-eight patients (mean age 21.1 +/- 3.5 years) at 19.9 +/- 3.2 years after atrial switch operations and 29 healthy controls were studied. The times from the onset of QRS to peak systolic strain (T epsilon) at the base of and the mid RV free wall, the ventricular septum (VS), and the left ventricular (LV) free wall were determined using tissue Doppler echocardiography. Intraventricular mechanical delay was defined as Delta T epsilon(RV-VS) and interventricular mechanical delay as Delta T epsilon(RV-LV). In patients, the magnitude of RV intra- and interventricular mechanical delay was correlated with cardiac magnetic resonance-derived RV volumes and ejection fractions (n = 26) and treadmill exercise testing parameters (n = 20). Compared with controls, patients had significantly longer Delta T epsilon(RV-VS) (48.1 +/- 50.9 vs 17.0 +/- 16.1 ms, p <0.001)>49 ms, control mean +/- 2SD), and 16 patients (57%) showed interventricular dyssynchrony (Delta T epsilon(RV-LV) >45 ms). In patients, RV intra- and interventricular mechanical delay was correlated negatively with the RV ejection fraction (both r = -0.42, p = 0.03) and percentage predicted maximum oxygen consumption (r = -0.50, p = 0.03, and r = -0.52, p = 0.02, respectively) and positively with minute ventilation/carbon dioxide production slope (r = 0.49, p = 0.03, and r = 0.56, p = 0.01, respectively). In conclusion, RV dyssynchrony is common in young adults after atrial switch operations and is associated with RV systolic dysfunction and impaired exercise performance.

Contraction pattern of the systemic right ventricle shift from longitudinal to circumferential shortening and absent global ventricular torsion.

OBJECTIVES: The aim of the present study was to characterize the contraction pattern of the systemic right ventricle (RV). BACKGROUND: Reduced longitudinal function of the systemic RV compared with the normal RV has been interpreted as ventricular dysfunction. However, longitudinal shortening represents only one aspect of myocardial deformation, and changes in contraction in other dimensions have not previously been described.

METHODS: Fourteen Senning-operated patients age 18.4 +/- 0.9 years (mean +/- SD) with transposition of the great arteries were studied. We compared the contraction pattern of the systemic RV with findings in the RV and left ventricle (LV) of normal subjects (n = 14) using tissue Doppler imaging and magnetic resonance imaging.

RESULTS: In the systemic RV free wall, circumferential strain exceeded longitudinal strain (-23.3 +/- 3.4% vs. -15.0 +/- 3.0%, p < 0.001) as was also the case in the normal LV (-25.7 +/- 3.1% vs. -16.5 +/- 1.7%, p < 0.001), opposite from the findings in the normal RV (-15.8 +/- 1.3% vs. -30.7 +/- 3.3%, p < 0.001). Strain in the interventricular septum did not differ from normal. Ventricular torsion was essentially absent in the systemic RV (0.3 +/- 1.8 degrees ), in contrast to a torsion of 16.7 +/- 4.8 degrees in the normal LV (p < 0.001).

CONCLUSIONS: In the systemic RV as in the normal LV, there was predominant circumferential over longitudinal free wall shortening, opposite from findings in the normal RV. This may represent an adaptive response to the systemic load. Noticeably, however, the systemic RV did not display torsion as found in the normal LV.

Left ventricular function in patients with transposition of the great arteries operated with atrial switch.

In patients operated with atrial switch for transposition of the great arteries (TGA), the left ventricle (LV) supports the pulmonary circulation and is thus pressure unloaded. Evaluation of LV function in this setting is of importance, as LV functional abnormalities have been documented and might contribute to development of symptoms. The ventricular contraction pattern in 14 Senning-operated TGA patients and 14 healthy controls was studied using tissue Doppler and magnetic resonance imaging. In the subpulmonary LV free wall, longitudinal strain was greater than circumferential strain (-23.6 +/- 3.6% vs. -19.1 +/- 3.2%, p = 0.002) as in the normal right ventricle (RV) (-30.7 +/- 3.3% vs. -15.8 +/- 1.3%, p < 0.001), but opposite to findings in the normal LV (-16.5 +/- 1.7% vs. -25.7 +/- 3.1%, p < 0.001).
Subpulmonary strain and strain rate values were intermediate between those in the normal LV and RV. Ventricular free-wall torsion was reduced in the subpulmonary LV compared with both the normal LV (5.7 +/- 3.2 degrees vs. 16.7 +/- 5.6 degrees , p < 0.001) and RV (5.7 +/- 3.2 degrees vs. 11.4 +/- 2.6 degrees , p < 0.05). Furthermore, early diastolic filling of the subpulmonary LV differed from that of the normal LV. The subpulmonary LV displayed predominantly longitudinal shortening, as did its functional counterpart, the normal RV. However, the degree and rate of both longitudinal and circumferential shortening were intermediate between those of the normal LV and RV. This could represent a partial adaptation to the reduced pressure load. Decreased ventricular torsion and diastolic abnormalities might indicate subclinical ventricular dysfunction.

Heart Disease on rise among Indian Youth

We are a nation of the young where 54 percent of our population is enjoying the prime of youth. But a black spot in this sunny picture is the increasing rate of heart disease among the youth. Today, the average age in which a person may suffer a heart attack has come down from 40 years to 30 years. And this is mainly a result of today’s changing lifestyles. In fact the rate of coronary heart disease in the Indian community - particularly in young men - is almost twice as high as their western counterparts.

Causes of The Increase
So what are the reasons or factors which have resulted in an increase in the number of heart patients in India? “Modern life style has proven to be the stimulus for the growth of heart diseases among the youth” says Dr Ashok Seth , Chief Invasive and Interventional Cardiology, Escorts Heart Institute. "Improper food habits, lack of physical activity and this coupled with high level of stress and increase in smoking and alcohol consumption are all classic risk factors which can put one high on the risk zone of coronary heart diseases. Sadly all these have become a part of the Indian youth’s life style.”
Not only college and school going students, but even working professionals have adopted the ways of this modern life style, and this has proved to be the instigator of heart diseases.

Food Culture

Junk food joints like Mc Donald’s, Pizza Hut etc. have become “hang out“ points not only for college students, but also amongst young professionals, who go for a quick bite to save time. We Indians already have a food culture which indulges itself in rich food which is fried in ghee, or foods as sweetmeats etc. This along with the addition of junk food to our diet and reduced physical activity has translated into increased heart risks.

The Biological Factor

The LDL (low density cholesterol) which is a result of such food habits puts us in the high risk zone as far as the heart diseases are concerned. The cholesterol gets deposited in the arteries making them narrower and narrower. As a result the blood supply to the heart gets thwarted. This leads to heart attacks.

However a thing which renders us Indians vulnerable to the risk is the biological fact that we Indians have narrower arteries than our European counterparts. According to Dr. Upendra Kaul, Director Interventional Cardiology and Cardiac Electrophysiology, Batra Hospital and Medical Research Centre, “It is important that one keeps a regular check on his\her weight. A BMI ( Body Mass Index) of more than 23 is bad news for your heart.”

Stress & Work Pressure

High-strung lifestyle is also another reason for the increase in Coronary Heart Diseases (CHD).

With the increase in the competition levels and the pressure to perform, youngsters are faced with the problem of stress at a very early stage. Things only deteriorate once they get into a job.

With the advent of MNC work culture in India, increased work pressure and increasing need for performance in the workplace, it has led to increased stress in the executive lifestyles. This type of a lifestyle increases the risk of developing heart disease by 10-15 times.

A sedentary life style since childhood, lack of proper exercise, genetic factors, fat and dietary conditions also dramatically raise the risk of developing coronary heart diseases.

Smoking

A Fad Smoking has become a fad in the young generation. It is seen as an in thing today and is considered as a fashion statement. However found to be the predominant cause of mortality and morbidity in the world. WHO estimates that globally 1.1 billion people smoke and about one-third are below the 16 years of age. Now let us look at why tobacco is harmful to health. Tobacco smoke contains a host of chemicals in the form of particles and gases which are potential carcinogens. However the most harmful toxins that are present in tobacco are Tar, Nicotine and Carbon Monoxide.

Harmful Effects Of Smoking

Whereas, nicotine is a highly addictive and toxic substance that diffuses into the blood stream causing various types of disorders. This has a variety of adverse effects on the body like increasing heart rate, blood pressure and it damages the inner lining of the blood supply to the heart causing endothelial dysfunction, which increases the risk of a person being exposed to coronary artery disease.

Carbon monoxide on its part is absorbed into the blood stream via the lungs and replaces oxygen from hemoglobin. This decreases the oxygen carrying capacity of the blood and decrease in the oxygen content results in damage of body cells. Says Dr Kaul "Professionals smoke because they feel it helps them to ease their tension. What they don’t think about is the adverse effect it would have on their health.”

Effects Of Alcohol

Alcohol is another factor which is responsible for the rise of coronary diseases amongst the youth. Alcohol has shown to depress the left ventricle of heart, which pumps blood into the body.

When this part of the heart is depressed, two things happen: The heart has to pump harder to get blood to your cells, and your cells and tissues don't get the supply needed for optimal functioning. If you also consider that strength training increases the thickness of the left ventricle, it only makes sense that anything that interrupts optimal functioning of this structure won't help you in the gym.

A recent investigation examined the relationship of alcohol consumption, heart disease and low-density lipoprotein (LDL) or "bad" cholesterol. LDL moves into cells, such as the fibroblasts in the walls of the arteries, where it forms the plaque and fatty deposits that clog arteries. The higher the ratio of LDL to HDL, the greater the risk of heart attack.

Conclusion

Couple this with all the above said factors such as calorie rich food and a sedentary life style and you have put yourselves in the maximum danger zone as far as CHD ( Coronary Heart Diseases) are concerned.

So if all these habits apply to you sit up and take notice. If you are young, it does not mean you are impervious to heart diseases. The only solution to the problem is leading a well balanced and healthy life style. And it is never too early when it comes to matters of the heart.

Cardiovascular disease

Cardiovascular disease can manifest itself in many different ways because the blood vessels transport blood to every single part of the body. The heart is the organ that pumps the blood around the body, and it also receives nutrients from the blood vessels (via the coronary vessels). Any interruption of the supply of blood containing nutrients and oxygen to one of the body's organs leads to functional impairment and, in the worst case scenario, the death of the tissue. One typical example is cardiac arrest, which occurs when the blood supply to the heart muscle is restricted. Cardiovascular disease can have any number of causes. Some people are born with a susceptibility to vascular disease (e.g. varicose veins), which can be alleviated by taking medication. Other people's heart and blood vessels can be damaged by external factors. The majority of vascular diseases these days, however, are caused by our modern-day lifestyles. The walls of the blood vessel are always in contact with the blood which flows through them, so they are most commonly affected by unhealthy lifestyles. If someone has an unfavourable haemogram, i.e. if their blood contains too much glucose, cholesterol, triglycerides (fats) or nicotine, this can put the blood vessels under an enormous amount of stress. Glucose adheres to the walls of the blood vessels and the blood constituents, and cholesterol and triglycerides also accumulate on the blood vessel walls. As a result, the blood clumps, the blood vessel walls "calcify", turn porous and can no longer perform their biological function properly. Nicotine also constricts the blood vessels, so they narrow and the amount of blood circulating the body is reduced. If the condition is aggravated by a lack of vessel-protecting substances, the damaged vessels lose their ability to regenerate. The consequences include arteriosclerosis, leg ulceration, dilation of the abdominal artery (aneurysm), cardiac insufficiency, cardiac arrest and stroke. Cardiovascular disease is still the number one cause of death in Germany and many other western industrial nations. Substances such as vitamins C and E, some of the B vitamins, secondary phytochemicals (such as the flavonoids which are contained in vegetables, reservatol in red wine, catechine in tea) and omega-3 fatty acids (fish) can protect the blood vessels. Sufficient physical activity also helps the blood vessels to retain their elasticity. People who change their lifestyle can therefore contribute to the prevention of cardiovascular disease. Once cardiovascular disease manifests, the range of therapies available are as varied as the symptoms themselves. The objective of any therapy is to normalise circulation (e.g. with medication to 'thin' the blood) and to repair or remove the damaged vessels. It is therefore important to take an integral approach to therapy which doesn't simply eliminate specific damage, but improves the entire cardiovascular system. After all, the damaged blood vessels are the underlying problem, not the strokes and heart attacks.