CAPITAL HEALTH

Inflammation plays a crucial role in the pathogenesis of arteriosclerosis, especially in acute coronary syndromes such as happen with a heart attack. And it was the very inability of ‘established’ risk factors such as high blood cholesterol (hypercholesterolemia), high blood pressure (hypertension) and smoking to fully explain the incidence of cardiovascular disease that has resulted in historically repeated calls to search out an infectious cause and the specific microbe behind it. Today, half of US heart victims have acceptable cholesterol levels, including HDL and LDL fractions, and 25% or more have none of the “risk factors” associated with heart disease, including smoking, high blood pressure or obesity, most of which are not inconsistent with being caused by infection to begin with. [1,2] Cholesterol itself was on the rise in Japanese blood during the very decade (1980-1989) when its incidence in coronary heart disease was on its way down. [22] So Nieto stressed the need to continue to look for an infectious disease behind heart disease. [3}

Which Disease?

Ever since a 1988 report of raised antibodies against Chlamydia pneumoniae in patients with heart disease, it was hoped that this microbe might be behind heart disease and atherosclerosis [28] Hurting this was the low incidence of atherosclerosis in the tropics despite Chlamydia’s high frequency there. [29]. Also Loehe, Bittman and other groups concluded that although Chlamydia, on occasion, might be present, it was not a causative factor in heart disease [30], because there was no correlation between the severity or extent of atherosclerosis and the involvement of chlamydial infection. Recently the Chlamydial hypothesis has been subject to a flurry of antibiotic trials, with mixed results, leaving some investigators to conclude that possibly Chlamydia doesn’t even play a role in atherosclerosis. [42] Certainly this was born out in two sizeable trials, one of which [47] had 1,187 participant. In neither trial [48] could any of the commonly thought of bacterial causes of heart problems – Chlamydia pneumonia and Helobacter pylori be correlated with cardiovascular disease. Nor could a virus. Also, in those trials which did show benefit antibiotics used (Azithromycin, Clarithromycin) are first line agents against certain forms of tuberculosis (fowl tuberculosis or Mycobacterium avium). Contrary to common belief, TB infections occur as a mixed infection with “atypical” TB in up to 11% of cases, even in HIV free individuals. [41] Today the antibiotic Rapamycin is used to coat coronary stents. [45] Rapamycin enhances the killing of mycobacteria like tuberculosis by human white blood cells called macrophages. [46]

Historical Associations

The association between active pulmonary tuberculosis and Acute Myocardial Infarction or heart attack has been reported and stubbornly ignored for around four and a half decades. Certainly, TB shares a more striking connection to heart disease than its nearest competitor, Chlamydia pneumonia. CDC maps for cardiovascular disease case rates bear a striking resemblance to comparable state and regional tuberculosis maps. [4,5]

Long before there was such a thing as a ‘heart specialist’ The National Tuberculosis Association created an offshoot called the American Heart Association (AHA). In one of its first bulletins, the American Heart Association came up with a long list of similarities between tuberculosis and heart disease. [17] And Ellis’s 1977 New England Journal of Medicine article [6], confirmed that the mortality rate for TB and heart disease were curiously about the same: 200 to 300 persons per 100,000.

By 1965, Rutgers investigators Livingston and Alexander-Jackson, working with sterile, post-catastrophic coronary artery and muscle specimens, established low-grade tubercular infection, staining ‘acid-fast’ (stains which did not decolorize when acid-alcohol was added) occuring in all ischemic heart specimens. [11] In that same year Russian investigators began generating their own proof that tuberculosis was causative in both atherosclerotic heart disease [18,19,20,21] and acute myocardial infarction (a heart attack) itself. [13,14,15].

Measuring Heart Trouble With Cardiac Enzymes In The Blood

Cases were soon on record of individuals with no cardiac risk factors, presenting with acute onset chest pain, ST elevation on their electrocardiogram (EKG), and elevated cardiac enzymes – all indicative of a heart attack with no other involvement than pulmonary tuberculosis [37]. As with its predecessor creatine kinase (CK-MB), today’s new enzymatic gold standard for detecting a heart attack, the troponins, are elevated in disseminated tuberculosis, an example of which can be found in TB’s role in acute pericarditis. [43]. Acute pericarditis, often not detected either until death was historically linked most commonly to Mycobacterium tuberculosis. In 1951, Christian [44] suggested that viral infection was more responsible for “idiopathic” (of unknown cause) or “benign” pericarditis. Such a viral cause, however, was never substantiated in many cases. Also, when it was found that the fatty substance (phospolipid) phosphatidylinositol  was not only housed itself inside TB’s cell wall, but was a potent coagulant and thrombin former as well – it further raised the question as to whether M. tuberculosis, by its very nature, lays down the conditions for the vessel clogging atherosclerosis behind heart disease and myocardial infarctions or heart attacks. [31]

Livingston and Alexander-Jackson [11] were far from the first ones to document lab evidence that TB can cause heart disease. Hektoen [7], Osler [8], and Schwartz [11], all documented lab and animal evidence to this effect. MacCallum [9] claimed that of all the infectious causes of heart disease, one one, tuberculosis, caused arteriosclerosis. At autopsy MacCallum cited 101 cases of advance tuberculous arteriosclerosis. In separate studies, Kossowsky [13], Tarakanova [14] and Ferrari-Sacco [15] all directly linked heart attacks with pulmonary tuberculosis.

Further evidence

There can no longer be any doubt that tubercular protein HSP-65 is involved in atherosclerosis. Xu [12] used it to cause experimental atherosclerosis in laboratory animals with normal cholesterol. George and Shoenfeld found it not only in atherosclerosis but fatty streak formation in cardiovascular blood vessels. [32] Mukherjee and De Benedictis showed also that the higher the antibodies against such tubercular protein in the body, the higher the possibility of “restenosis” or future closure of heart vessels. Also Afek proved that the higher the amount of tuberculoprotein (HSP-65) administered, the larger the area of vessel clogging atherosclerosis, even despite a low-fat diet. [34] Xu saw similar changes in New Zealand White Rabbits. [35] Xu’s rabbits had normal serum cholesterol, but when injected with tubercular protein, their arteries soon developed the classic features of arteriosclerosis in humans – both with regards to inflammatory cell accumulation and smooth cell proliferation. [IBID]. The only finding missing from Xu’s animals were “foam cells” – fat laden tissue white blood cells called macrophages in which tuberculosis lives and thrives. Xu remedied this by subjecting his animals to a cholesterol rich diet in addition to tubercular protein. this combination produced classic human heart disease, with foam cells. Xu continued to find sustained antibodies to HSP-65 in human subjects with the severe atherosclerosis predictive of mortality. [49] By 2004 Mandal and Xu even confirmed a positive association between high levels of antibodies to HSP-65, which are cytotoxic, and the vexing atrial fibrillation that often accompanies cardiac surgery. [50]

Present day heart disease “markers” have been suggest as indicators of possible heart disease, even in the 25 million US patients who have none of its “risk factors”. These include blood test for C-Reactive Protein (CRP), interleukin-6 and homocysteine [39] – all of which are similarly elevated in tuberculosis. [32,33,34,40,36].

Although blood cholesterol seems an imperfect criterion by itself for determining coronary heart disease, its intimate interaction with TB is unique. Tuberculosis is the only microorganism to depend on cholesterol for its destructive pathogenesis, and it relies upon cholesterol to enter the body’s white blood cell macrophages. [23] The tuberculous bacilli alone is able to produce [24], esterify [25], take up, modify, accumulate [26], and promote the deposition of, and release [27] of cholesterol. The statins, among the most popular drugs in America (Lipitor), inhibit Coenzyme-A compounds, and as such lower serum cholesterol levels. But they do more. Specifically, when macrophages were depleted of cholesterol by these agents, it hinders tuberculosis’s entrance into the body’s macrophages that TB likes to house in, thrive in, and depends upon. [23]

Nieto concludes that the introduction of antibiotic therapies in the 1940′s and 1950′s could have contributed to the decline of heart disease and heart attacks, and so, by 2000, the CDC found that 14% of the cardiologists in Alaska and West Virginia treated heart patients with antibiotics for angina, heat attacks, angioplasty or after by-pass surgery.

Conclusion

In Tuberculosis in Disguise, Rab and Rahman report cases of congestive heart failure and ischemic heart disease (IHD) with chest pain, raised erythrocyte sedimentation rate, leukocytosis (elevated white cell count) and inverted T-waves across the chest leads in an Electrocardiogram – otherwise indistinguishable from a heart attack, which turned out to be miliary (systemic) tuberculosis. [38]

Though more than 120 years have passed since its discovery Mycobacterium tuberculosis is still the leading cause of infectious death globally due to a single infectious agent. At least a staggering 1.7 million around the globe die of tuberculosis each year, while another 1.9 million are infected and at risk for active tubercular disease. [16] The World Health Organization [WHO] estimates that 1/3 of the planet has contracted TB. It would take such a disease of such magnitude to adequately explain the scope of cardiovascular disease, which affects, according to the CDC (Centers for Disease Control) about 61 million people, or almost one-fourth of the population of the US alone. Almost 6 million US hospitalizations each year are due to cardiovascular disease, which has become an equal opportunity disease that is now both the leading cause of death among women as well as the general US population.

There is at least as much, and probably much more evidence that Mycobacteria, particularly Mycobacterium tuberculosis causes cardiovascular disease than there is regarding Chlamydia Pneumoniae. Yet oddly, to this point Chlamydia has been pursued in therapeutic antibiotic trial after trial…………with not one such trial directed towards tuberculosis.

 

References

1. Benson RL, Smith KG. Experimental arteritis and arteriosclerosis associated with          streptococcal      inoculations. Arch Pathol 1931;12:924–40.

2. Thom DH, Grayston JT. Association of prior infection with Chlamydia    pneumoniae and angiographically demonstrated coronary artery disease. JAMA 1992;268:68–72.

3. Nieto FJ. Infections and atherosclerosis: new clues from an old hypothesis. Am J Epidemiol 1998;148(10):937–48.

4. CDC Map: TB case rates, United States, 2001. Atlanta Georgia: US Department of Health, Education and Welfare CDC; 2001.

5. CDC Map total cardiovascular disease – 1995 death rate. Atlanta Georgia: US Department of Health, Education Welfare CDC; 1995.

6. Ellis JG. Plague tuberculosis and plague atherosclerosis. The New England J Med 1977;296(12):695.

7. Hektoen L. The vascular changes of tuberculous meningitis. J Exper Med 1986:112.

8. Osler W. Diseases of the arteries. In: Osler W, MacCrae T, editors. Modern medicine Its theory and practice in original contributions by Americans and foreign authors, vol. 4. Philadelphia, PA: Lea & Fabiger; 1908. p. 426–47.

9. MacCallum WG. Acute and chronic infections as etiological factors in arteriosclerosis. In: Cowdry EV, editor. Arteriosclerosis A survey of the problem. New York: MacMillan Co; 1933. p. 355–62.

10. Schwartz P. Amyloid degeneration and tuberculosis in the aged. Gerontologia 1972;18(5-6):321–62.

11. Livingston V. Cancer: a new breakthough. Los Angeles: Nash Publishing; 1972.

12.  Xu Q. Dietrich Induction of arteriosclerosis in normocholesterolemic mice and rabbits by immunization with heat shock protein 65. Arterioscler Thromb 1992;12:789–99.

13. Kossowsky WA, Rafii S. Letter: acute myocardial infarction in miliary tuberculosis. Ann Intern Med 1975;82(6):813–4.

14. Tarakanova KN, Terent’eva GM. Myocardial infarct in patients with pulmonary tuberculosis. Probl Tuberk 1972;50(4):90–1.

15. Ferrari-Sacco A, Ferraro U. Myocardial Infarct and Pulmonary Tuberculosis. Discussion of 2 cases of myocardiocoronary disease appearing during hospitalization in a sanatorium. Minerva Cardioangiol 1966;14(8):465–75.

16. Dye C, Scheele S. Global burden of tuberculosis: estimated incidence, prevalence, and mortality by country. JAMA 1999;282:677–86.

17. AHA Similarity of tuberculosis and heart disease. Bull Am Heart Assoc 1927;2(5):22.

18. Bruade VI. Cardiovascular diseases in conjunction with pulmonary tuberculosis (pathological-anatomical findings). Sov Med 1966;29(12):104–7.

19. Kamyshnikova VS, Kolb VG. Biochemical factors involved in atherogenesis in pulmonary tuberculosis. Probl Tuberk 1984;11:48–52.

20. Kazykhanov NS. Lung tuberculosis in patients with atherosclerosis. Sov Med 1965;28(8):37–44.

21. Kazykhanov NS. Arteriosclerosis in patients with pulmonary tuberculosis. Kardiologiia 1967;7(10):137.

22. Okayama A. Ueshima changes in total serum cholesterol and other risk factors for cardiovascular disease in Japan, 1980–1989. Int J Epidemiol 1993;22:1038–47.

23. Gatfield J, Pieters J. Essential role for cholesterol in entry of mycobacteria in macrophages. Science 2000;288:1647–750.

24. Lamb DC, Kelly DE. A sterol biosynthetic pathway in mycobacterium. FEBS Lett 1998;437(1-2):142–4.

25. Kondo E, Kanai K. Accumulation of cholesterol esters in macrophages incubated with mycobacteria in vitro. Jpn J Med Sci Biol 1976;29(3):123–37.

26. Av-Gay Y, Sobouti R. Cholesterol is accumulated by mycobacteria but its degradation is limited to non-pathogenic Heart disease: the greatest ‘risk’ factor of them all 777 fast growing mycobacteria. Can J Microbiol 2000;46(9):826–31.

27. Kamyshnikov VS, Kolb VG. Lipid metabolism and atherogenesis in tuberculosis in experimental animals. Probl Tuberk 1993;4:53–5.

28. Gurfinkel E, Bozovich G. Chlamydia pneumoniae: inflammation and instability of the atherosclerotic plaque. Atherosclerosis 1998;140(Suppl 1):31–5.

29. Stille W, Dittmann R. Arteriosclerosis as a sequela of chronic Chlamydia pneumoniae infection. Herz 1998;23(3):185–92.

30. Loehe F, Bittmann I. Chlamydia pneumoniae in atherosclerotic lesions of patients undergoing vascular surgery. Ann Vasc Surg 2002;16(4):467–73.

31. Rota S  Rota S  Mycobacterium tuberculosis Complex in Atherosclerosis  Acta. Med. Okayama 59:6 pp.247-251 2005

32. George J, Shoenfeld Y. Enhanced fatty streak formation in C57BL/6J Mice by immunization with heat shock protein-65 arteriosclerosis. Thromb Vasc Biol 1999;19:505–10.

33. Mukherjee M. De Benedictis association of antibodies to heat-shock protein-65 with percutaneous transluminal coronary angioplasty and subsequent restenosis. Thromb Haemost 1996;75(2):258–60.

34. Afek A, George J. Immunization of low-density lipoprotein receptor deficient (LDL-RD) mice with heat shock protein 65 (HSP-65) promotes early atherosclerosis. J Autoimmun 2000;14(2):115–21.

35. Xu Q, Kleindienst R. Increased expression of heat shock protein 65 coincides with a population of infiltrating T lymphocytes in atherosclerotic lesions of rabbits specifically responding to heat shock protein 65. J Clin Invest 1993;91:2693–702.

36. Markkansen T, Levanto A. Folic acid and vitamin B12 in tuberculosis. Scand J Haemat 1967;4:283–91.

37. Bakalli A  Osmani B  Acute myocardial infarction and pulmonary tuberculosis in a young female patient: a case report Cases Journal 1: 246 2008

38.  Rab SM, Rahman M. Tuberculosis in disguise. Brit J Dis Chest 1967;61:90–4.

39. Wilson PW. Homocysteine and coronary heart disease: how great is the hazard? JAMA 2002;288(16):2042–3.

40. Bajaj G, Rattan A. Prognostic value of ‘C’ reactive protein in tuberculosis. Indian Pediatr 1989;26(10):1010–3.

41. Tsukamura M, Mizuno S. Occurrence of Mycobacterium tuberculosis and strains of the Mycobacterium avium- M. intracellulare complex together in the sputum of patients with pulmonary tuberculosis. Tubercle 1981;62:43-46.

42. Pislru S Van de Werf F  Editorial: Antibiotic Therapy for Coronary Artery Disease. Can Wizard Change It All? JAMA. 2003;290: 1515-1516

43.  Imazio M Demichelis B  Cardiac Troponin I in Acute Pericarditis  Journal of the American College of Cardiology Vol.42, No. 12 pp. 2144-2148  2003

44. Christian HA Nearly ten decades of interest in idiopathic pericarditis  Am. Heart J. 42:654 1961

45. Li YL  Wan Z  Comparison of Sirolimus- and Paclitaxel-Eluting Stents in Patients Undergoing Primary Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction: A Meta-analysis of Randomized Trials. Clin Cardiol. 2010 Sep;33(9):583-90.

46. Floto AF  Sarkar S Perlstein EO Addendum: Small Molecule Enhancers of Rapamycin-Induced TOR Inhibition Promote Autophagy, Reduce Toxicity in Huntington’s Disease Models and Enhance Killing of Mycobacteria by Macrophages. Autophagy  Landes Bioscience 3:6, 620-622; November/December 2007.

47. Haider AW Wilson PW  The association of seropositivity to Helicobacter pylori, Chlamydia pneumonia, and cytomegalovirus with risk of cardiovascular disease: a prospective study. J. Am Coll Cardiol. 2002 Oct 16;40(8):1408-13.

48.  Ridker PM Kundsin RB Prospective study of Chlamydia pneumonia IgG seropositivity and risks of future myocardial infarction. Circulation 1999 Mar 9;99(9):1161-4.

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Heart disease encompasses a myriad of heart conditions, such as coronary artery disease, heart attack and heart failure, among other less common diseases. According to the Centers for Disease Control, heart disease is the leading cause of death in most ethnic groups throughout the U.S. These are harsh but real statistics that make heart health well worth addressing. Although heart disease isn’t 100 percent preventable, there are preventative measures, lifestyle changes, and other ways to keep you and your loved ones well, and your heart health at its best. It is also important to be aware of the signs and symptoms of heart disease, in order to seek treatment quickly and to ensure the best possible outcome if something goes wrong.

 

Coronary Artery Disease

According to the Heart, Lung and Blood Institute, coronary artery disease is a condition where plaque builds up in the coronary arteries, cutting off the supply of oxygen-rich blood to the heart. Coronary artery disease often results in heart attack, and is the leading killer of both men and women in the U.S. In 2006 alone, more than 600,000 people died from this disease — and those numbers continue to climb today.

 

Preventing Coronary Artery Disease

The most common type of heart disease in the U.S. is coronary artery disease (CAD), notes the Centers for Disease Control. The risk for coronary artery disease can be greatly reduced through certain lifestyle changes. The largest preventative factor is reducing cholesterol and blood pressure. Some of the lifestyle changes suggested for people at risk for CAD are exercise, a healthy diet, and maintaining a healthy weight. Some of the most common risk factors include diabetes, obesity or being overweight, and having high cholesterol and blood pressure.

If maintaining a healthy diet and exercise routine proves difficult for your loved one, find exercises that cater to their interests and physical abilities, such as a stroll through the park, a leisurely swim or water aerobics class, playing a game of tennis, practicing yoga, or biking. If appropriate, also consider low-impact, seated exercise, like the Sit And Be Fit program. Setting aside daily time for physical activity can be a great opportunity for you and your family to spend time with your loved one, or for them to meet friends with similar interests.

Although the above-mentioned lifestyle changes are not a 100 percent guarantee in preventing CAD, they can lead to a happier, healthier life for your loved one, and a more rapid recovery from illness and/or injury.

 

Signs & Symptoms of Coronary Artery Disease

The leading symptom of coronary artery disease is angina, more commonly known as chest pain. Angina can be experienced in a range of ways, from pain, pressure or even squeezing in the chest — but may also be felt in the shoulders, neck, arms or back, according to the Heart, Lung and Blood Institute. Shortness of breath, an irregular heartbeat and fatigue are also early signs of CAD. If you believe you may be suffering from coronary artery disease, consult your doctor promptly. It is important to see your doctor if you start experiencing symptoms, because a prompt diagnosis and immediate treatment means an easier recovery.

 

Heart Attack

A heart attack occurs when blood flow to a certain section of the heart is blocked. This blockage can result for any number of reasons, with the most frequent being plaque build-up and high cholesterol levels. The Heart, Lung and Blood Institute explains if any section of the heart doesn’t receive blood flow again — and quickly — it may suffer permanent damage and will often die. Each year, about 1.1 million people in the U.S. have heart attacks, and almost half of those heart attacks result in death.

 

Prevention

Living a healthy lifestyle is the best way to prevent heart attack. The American Heart Association cites the following as the best preventative measures: quit smoking, choose good nutrition, reduce cholesterol, maintain daily physical activity and a healthy weight, manage diabetes, reduce stress and limit alcohol intake.

Some of these habits may be hard to break — but the best care you can give your loved one is to help them choose a healthy lifestyle by making obtainable daily goals. Exercise doesn’t have to mean time at the gym, it can be as simple as moving more. Good nutrition can start with small steps, such as drinking more water and choosing healthier grains. Embracing a healthy lifestyle requires a serious commitment, but the choice to live better is worth it.

 

Signs & Symptoms of a Heart Attack

In the event that you or a loved one suffers a heart attack, knowing the signs and symptoms can save your life. Most people commonly recognize chest pain as an indicator, but are not aware that many other symptoms can be present. The Centers for Disease Control lists the following as warning signs of a heart attack: chest pain lasting for more than a few minutes, or chest pain that comes and goes; pain or discomfort in one or both arms, the back, neck, jaw or stomach; shortness of breath; cold sweats; nausea; feeling light-headed. A heart attack feels different to each person. If you’re experiencing any of these symptoms and believe you’re having a heart attack, call 9-1-1 immediately. It is crucial to recognize the myriad of symptoms associated with a heart attack — in order to receive immediate treatment to save the heart and prevent further complications.

 

Heart Failure

As defined by the Heart, Lung, and Blood Institute, heart failure occurs when the heart can’t pump enough blood throughout the body. Heart failure doesn’t mean that the heart has stopped, but it does mean that quick medical attention is a necessity. About 5.7 million people in the U.S. suffer from heart failure, resulting in about 300,000 deaths per year.

 

Prevention

People at high risk for heart failure include diabetics, those who are obese, and those suffering from coronary artery disease. Whether you’re at risk or not, taking care of your heart to prevent heart failure is essential. The Heart, Lung and Blood Institute cites the following as key preventative measures: maintaining a healthy weight; eating a diet full of lean meats, beans, fruits and vegetables; avoiding saturated fat, cholesterol and sodium; refraining from smoking and heavy drinking; engaging in physical activity regularly. Following a heart-healthy diet, as well as exercising routinely will keep your loved one step ahead of heart failure. It is crucial to keep the heart muscle healthy in order to keep the rest of the body healthy.

 

Heart Failure Signs & Symptoms

If you’re suffering from heart failure, you’ll most likely notice certain signs and symptoms. The symptoms of heart failure are not as pronounced as those of a heart attack, and therefore go unnoticed, and often for long periods of time. If you’re fatigued, have shortness of breath, are experiencing swelling in the ankles, legs, abdomen and veins in the neck, you may be suffering from heart failure, explains the Centers for Disease Control. As the heart weakens, it may be exhausting for you to carry out simple daily tasks, like bathing or putting away laundry. If you’re experiencing any of these symptoms, consult a doctor as soon as possible.

There is no known cure for heart disease, heart attack, and heart failure, but preventing ailments of the heart can be as easy as basic lifestyle changes. As scientific research and medical studies continue to improve, the emphasis on exercise and a healthy diet grows. No matter your age, risk factors, or genetics, taking care to prevent heart disease and keep heart health optimal is essential.

There are many types of heart disease, but this article will explore five types of heart disease that are common to happen. Hopefully, this article can add your knowledge concerning this leading cause of death disease.

#1 congenital heart disease

There is a fallacy of thinking that many people do when they believe that all heart disease is brought about by outside factors or that it needs some periods of time for heart disease to build up. This is, of course, not true as one of the most common types of heart disease is congenital heart disease.

The term congenital or hereditary heart disease refers to heart disease which is passed down through the family, and this is considered as being a congenital type of heart disease as it is principally inevitable and unpreventable. If you have an account of early heart disease in your family then you also are at danger for congenital heart disease.

The most first-degree family members that you have who have endured from heart disease, such as your mother, father, brother, sister and so on, in particular those who experienced it at a younger age, the higher your risk of getting it as well.

Although congenital heart disease can be caused by many factors, some of them are actually preventable. For example if heart disease is clustering in your family, then it may just be because of the way that your family lives, including unhealthy practices such as poor diet, little or no exercise, and smoking. All of these aspects can contribute to heart disease and can create the sequence of congenital heart disease.

# 2 congestive heart failure

Congestive heart failure is when the heart does not pump adequate blood to the other organs in the body. Congestive heart failure can often result from heart disease and constricted arteries. Congestive heart failure results in a heart which works a lot less efficiently than it should and can make further problems. Symptoms regularly consist of swelling and edema, shortness of breath, and kidney problems which in turn can lead to mysterious weight gain. Even elevated blood pressure and alcohol abuse can lead to congestive heart failure.

A patient may be examined for congestive heart failure if they have suffered from heart disease in the past, are alcoholic, have a family history of heart problems or show one or all of the symptoms that are caused by congestive heart failure. There are choices of examinations that aid a doctor in diagnosing this heart crisis. Treatment should begin without delay, starting with changes to diet and exercise, as patients should abolish salt from the diet altogether and sternly limit their fluid intake. Further treatment should be done by a professional.

#3 coronary heart disease

Coronary heart disease is the most frequent type of heart disease of all, and is also the leading reason of heart attacks. Coronary heart disease is a term that refers to damage to the heart that happens because its blood supply is decreased, and what happens here is that fatty deposits build up on the linings of the blood vessels that provide the heart muscles with blood, resulting in them narrowing. This narrowing decreases the blood supply to the heart muscles and causes pain that is identified as angina.

There are a few factors which are considered as being responsible causes of coronary heart disease. One in particular is high cholesterol that can increase fat concentration in your blood and create the building up of fatty deposits. Another one of the major factors of coronary heart disease is cigarette and tobacco smoke, as a smoker’s risk of getting heart disease is two times that of a nonsmoker, and studies have actually revealed that after five years of quitting smoking, the risk of developing heart disease is the same as that of someone who had never smoked in their life.

#4 pulmonary heart disease

Pulmonary heart disease is heart disease that comes from a lung, or pulmonary, disorder, or a complication of lung problems where the blood flow into the lungs is slowed or even totally blocked, resulting in increased pressure on the lungs. There are a number of different symptoms that typically come with pulmonary heart disease, such as shortness of breath, syncope, dyspnoea, and chest pain.

It is a state which is often misdiagnosed, and has frequently progressed to late stages by the time that it is actually correctly diagnosed. It has been previously chronic and untreatable with a poor survival rate. However, there are now numerous new treatments which are accessible which have extensively improved the overall prognosis of this disease.

#5 rheumatic heart disease

Rheumatic heart disease frequently derives from strep throat infections. This can be a reason for alarm for many because strep throat, while often preventable, is a quite common condition that affects many people who do not treat a minor sore throat infection in time. However, there is no reason to be because rheumatic heart disease that comes from strep throat is fairly rare. Actually, the sheer volume of cases of rheumatic heart disease has decreased considerably since the 1960′s.

If rheumatic fever, which happens due to chronic strep throat, is contracted and leads to rheumatic heart disease, the situation can be treated in a way that is much easier than the common treatments for other types of heart disease. This treatment usually involves taking cortisteroid anti-inflammatory medication to reverse any possible cardiac problems the fever might make. This does not rule out the risk for the requirement for more advanced treatment such as surgery, but it does signify the probability for a simple, yet effective treatment.

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