heart attack and how to help the victims

about heart atack

A heart attack occurs when blood flow to a section of heart muscle becomes blocked. If the flow of blood isn’t restored quickly, the section of heart muscle becomes damaged from lack of oxygen and begins to die.

Heart attack is a leading killer of both men and women in the United States. But fortunately, today there are excellent treatments for heart attack that can save lives and prevent disabilities. Treatment is most effective when started within 1 hour of the beginning of symptoms. If you think you or someone you’re with is having a heart attack, call 9–1–1 right away.

Overview

Heart attacks occur most often as a result of a condition called coronary artery disease (CAD). In CAD, a fatty material called plaque (plak) builds up over many years on the inside walls of the coronary arteries (the arteries that supply blood and oxygen to your heart). Eventually, an area of plaque can rupture, causing a blood clot to form on the surface of the plaque. If the clot becomes large enough, it can mostly or completely block the flow of oxygen-rich blood to the part of the heart muscle fed by the artery.

Heart With Muscle Damage and a Blocked Artery

Figure A is an overview of a heart and coronary artery showing damage (dead heart muscle) caused by a heart attack. Figure B is a cross-section of the coronary artery with plaque buildup and a blood clot.

During a heart attack, if the blockage in the coronary artery isn’t treated quickly, the heart muscle will begin to die and be replaced by scar tissue. This heart damage may not be obvious, or it may cause severe or long-lasting problems.

Severe problems linked to heart attack can include heart failure and life-threatening arrhythmias (irregular heartbeats). Heart failure is a condition in which the heart can’t pump enough blood throughout the body. Ventricular fibrillation is a serious arrhythmia that can cause death if not treated quickly.

Get Help Quickly

Acting fast at the first sign of heart attack symptoms can save your life and limit damage to your heart. Treatment is most effective when started within 1 hour of the beginning of symptoms.

The most common heart attack signs and symptoms are:

• Chest discomfort or pain—uncomfortable pressure, squeezing, fullness, or pain in the center of the chest that can be mild or strong. This discomfort or pain lasts more than a few minutes or goes away and comes back.
• Upper body discomfort in one or both arms, the back, neck, jaw, or stomach.
• Shortness of breath may occur with or before chest discomfort.
• Other signs include nausea (feeling sick to your stomach), vomiting, lightheadedness or fainting, or breaking out in a cold sweat.

If you think you or someone you know may be having a heart attack:

• Call 9–1–1 within a few minutes—5 at the most—of the start of symptoms.
• If your symptoms stop completely in less than 5 minutes, still call your doctor.
• Only take an ambulance to the hospital. Going in a private car can delay treatment.
• Take a nitroglycerin pill if your doctor has prescribed this type of medicine.
• Put an aspirin under your tongue. Aspirin reduces blood clotting and can help keep a heart attack from getting worse. But don’t delay calling 9–1–1 to take an aspirin.

this article was quoted from nhlbi.nih,gov

Heart Cancer Treatment

Cancer of the heart. Heart cancer is very rare and develops in the tissues of the heart. It is also known as a cardiac sarcoma or an angiosarcoma. The general belief is that cells that divide regularly (tissues that are constantly regenerating such as the skin and bones) are more likely to develop cancer than heart tissue who's cells generally don't divide at all. (Source: WD Writers)

Causes of Heart cancer

Chest Pain: Differential Diagnosis
(In a Page: Signs and Symptoms)

• Cardiovascular etiologies
  –Myocardial infarction
  –Angina
  –Acute coronary syndrome
  –Pulmonary embolus
  –Pericarditis
  –Arrhythmias
  –Mitral valve prolapse
  –Aortic stenosis
  –Aortic dissection
  –Cardiac tamponade
• Pulmonary etiologies
  –Pneumonia
  –COPD
  –Asthma
  –Pneumothorax
  –Tension pneumothorax
  –Hemothorax
  –Empyema
  –Pneumomediastinum
  –Lung cancer
• Gastrointestinal etiologies
  –Esophagitis/GERD
  –Gastritis
  –Peptic ulcer disease
  –Perforated ulcer
  –Esophageal spasm
  –Pancreatitis
  –Esophageal rupture
  –Pneumoperitoneum
• Musculoskeletal etiologies
  –Muscle strain or spasm
  –Intercostal muscle spasm
  –Costochondritis
  –Trauma (e.g., rib fracture)
• Zoster
• Cancer (e.g., lymphoma)
• Panic disorder
• Less common etiologies include Tietze's syndrome, Pott's disease (tuberculosis of the spine), xyphodenia, cholecystitis, peritonitis, liver cancer, and hepatitis

Chest Pain: Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)

• Musculoskeletal
  –Sharp, stabbing pain that is usually very well localized, often worsened by deep breath or cough
  –Costochondritis: Tender parasternal pain at insertion of ribs into cartilage en route to sternum; increases with palpation or mild chest compression (possibly postviral)
  –Injury to chest wall

• Pulmonary
  –Very common cause, usually associated with respiratory symptoms: Shortness of breath, cough, exercise intolerance
  –Asthma (most common), often only EIA; may have personal/family history of atopy (asthma, eczema, seasonal allergies); shortness of breath is usually primary complaint, with feeling of chest tightness/pain as a secondary symptom
  –Pleuritic chest pain: Sharp, stabbing pain with deep breaths, indicates pleural space inflammation, probably postinfectious (especially viral)
  –Pneumonia: Chest pain secondary to cough or pleural involvement
  –Pneumothorax can occur spontaneously, especially in tall, thin athletes

• Gastrointestinal
  –GERD and PUD: Burning, substernal pain with eating, worse at night
  –Rarely pancreatitis (with back pain too), cholecystitis, hiatal hernia, hepatitis

• Cardiac: Rare in children
  –Precordial catch syndrome: Sharp, brief (seconds) chest pain usually associated with rising from lying or sitting; unclear etiology, but of no significance
  –Pericarditis: Inflammation of the pericardium; often postviral, may represent connective tissue/autoimmune, cancer, bacterial infection (very ill appearing with fever), or post-cardiac surgery; patients often lean forward to decrease the pain
  –MI (rare): Congenital coronary anomaly, post-Kawasaki, cocaine use, hypertrophic cardiomyopathy
  –Aortic dissection: Consider if features or history of Marfan syndrome is present

Chest pain: Medical causes
(Handbook of Signs & Symptoms (Third Edition))

Treatment

• Attention to airway, breathing, and circulation
• All patients with suspected coronary artery disease should initially be treated with supplemental O₂, aspirin, and nitroglycerin; morphine may be added if pain does not subside
• 
  
• If an acute myocardial infarction is suspected, β-blockers, ACE inhibitors, heparin (usually low molecular weight heparin, enoxaparin), thrombolytic therapy or primary angioplasty (PTCA), and/or glycoprotein IIb/IIIa inhibitors (e.g., eptifibatide, abciximab, or tirofiban) may be indicated
• Treat other etiologies as appropriate (e.g., antiarrhythmics and/or cardioversion for arrhythmias, pericardiocentesis for cardiac tamponade, H2 blockers or PPIs for GERD and peptic ulcer disease, antibiotics for pneumonia, bronchodilators and steroids for asthma)
• Emergent surgery for aortic dissections that involve the aortic arch proximal to left subclavian artery (type A); strict blood pressure control for type B dissections that only involve the aorta distal to left subclavian artery

this article was quoted from wrongdiagnosis.com

Preventing Lung Cancer

Definition of lung cancer: Cancer that forms in tissues of the lung, usually in the cells lining air passages. The two main types are small cell lung cancer and non-small cell lung cancer. These types are diagnosed based on how the cells look under a microscope.

Estimated new cases and deaths from lung cancer (non-small cell and small cell combined) in the United States in 2007:

	New cases: 213,380
	Deaths: 160,390

What causes lung cancer?

Smoking

The incidence of lung cancer is strongly correlated with cigarette smoking, with about 90% of lung cancers arising as a result of tobacco use. The risk of lung cancer increases with the number of cigarettes smoked over time; doctors refer to this risk in terms of pack-years of smoking history (the number of packs of cigarettes smoked per day multiplied by the number of years smoked). For example, a person who has smoked two packs of cigarettes per day for 10 years has a 20 pack-year smoking history. While the risk of lung cancer is increased with even a 10 pack-year smoking history, those with 30 pack-year histories or more are considered to have the greatest risk for the development of lung cancer. Among those who smoke two or more packs of cigarettes per day, one in seven will die of lung cancer.

Pipe and cigar smoking can also cause lung cancer, although the risk is not as high as with cigarette smoking. While someone who smokes one pack of cigarettes per day has a risk for the development of lung cancer that is 25 times higher than a nonsmoker, pipe and cigar smokers have a risk of lung cancer that is about five times that of a nonsmoker.

Tobacco smoke contains over 4,000 chemical compounds, many of which have been shown to be cancer-causing, or carcinogenic. The two primary carcinogens in tobacco smoke are chemicals known as nitrosamines and polycyclic aromatic hydrocarbons. The risk of developing lung cancer decreases each year following smoking cessation as normal cells grow and replace damaged cells in the lung. In former smokers, the risk of developing lung cancer begins to approach that of a nonsmoker about 15 years after cessation of smoking. For more, please read the Smoking and Quitting Smoking article.

Passive smoking

Passive smoking, or the inhalation of tobacco smoke from other smokers sharing living or working quarters, is also an established risk factor for the development of lung cancer. Research has shown that non-smokers who reside with a smoker have a 24% increase in risk for developing lung cancer when compared with other non-smokers. An estimated 3,000 lung cancer deaths occur each year in the U.S. that are attributable to passive smoking.

Asbestos fibers

Asbestos fibers are silicate fibers that can persist for a lifetime in lung tissue following exposure to asbestos. The workplace is a common source of exposure to asbestos fibers, as asbestos was widely used in the past for both thermal and acoustic insulation materials. Today, asbestos use is limited or banned in many countries including the Unites States. Both lung cancer and mesothelioma (a type of cancer of the pleura or of the lining of the abdominal cavity called the peritoneum) are associated with exposure to asbestos. Cigarette smoking drastically increases the chance of developing an asbestos-related lung cancer in exposed workers. Asbestos workers who do not smoke have a fivefold greater risk of developing lung cancer than non-smokers, and those asbestos workers who smoke have a risk that is 50 to 90 times greater than non-smokers.

Radon gas

Radon gas is a natural, chemically inert gas that is a natural decay product of uranium. It decays to form products that emit a type of ionizing radiation. Radon gas is a known cause of lung cancer, with an estimated 12% of lung cancer deaths attributable to radon gas, or 15,000 to 22,000 lung cancer-related deaths annually in the U.S. As with asbestos exposure, concomitant smoking greatly increases the risk of lung cancer with radon exposure. Radon gas can travel up through soil and enter homes through gaps in the foundation, pipes, drains, or other openings. The U.S. Environmental Protection Agency estimates that one out of every 15 homes in the U.S. contains dangerous levels of radon gas. Radon gas is invisible and odorless, but can be detected with simple test kits.

Familial predisposition

While the majority of lung cancers are associated with tobacco smoking, the fact that not all smokers eventually develop lung cancer suggests that other factors, such as individual genetic susceptibility, may play a role in the causation of lung cancer. Numerous studies have shown that lung cancer is more likely to occur in both smoking and non-smoking relatives of those who have had lung cancer than in the general population. Recent research has localized a region on the long (q) arm of the human chromosome number 6 that is likely to contain a gene that confers an increased susceptibility to the development of lung cancer in smokers.

Lung diseases

The presence of certain diseases of the lung, notably chronic obstructive pulmonary disease (COPD), is associated with a slightly increased risk (four to six times the risk of a nonsmoker) for the development of lung cancer even after the effects of concomitant cigarette smoking are excluded.

Prior history of lung cancer

Survivors of lung cancer have a greater risk than the general population of developing a second lung cancer. Survivors of non-small cell lung cancers (NSCLCs, see below) have an additive risk of 1-2% per year for developing a second lung cancer. In survivors of small cell lung cancers (SCLCs) the risk for development of second cancers approaches 6% per year.

Air pollution

Air pollution, from vehicles, industry, and power plants, can raise the likelihood of developing lung cancer in exposed individuals. Up to 1% of lung cancer deaths are attributable to breathing polluted air, and experts believe that prolonged exposure to highly polluted air can carry a risk similar to that of passive smoking for the development of lung cancer.

How can lung cancer be prevented?

Smoking cessation is the most important measure that can prevent lung cancer. Many products, such as nicotine gum, nicotine sprays, or nicotine inhalers, may be helpful to people trying to quit smoking. Minimizing exposure to passive smoking is also an effective preventive measure. Using a home radon test kit can identify and allow correction of increased radon levels in the home, which can also cause lung cancers. Methods that allow early detection of cancers, such as the helical low-dose CT scan, may also be of value in the identification of small cancers that can be cured by surgical resection and prevention of widespread , incurable metastatic cancer.

Lung Cancer At A Glance

• Lung cancer is the number one cause of cancer deaths in both men and women in the U.S. and worldwide.
• Cigarette smoking is the principal risk factor for development of lung cancer.
• Passive exposure to tobacco smoke can also cause cancer.
• The two types of lung cancer, which grow and spread differently, are the small cell lung cancers (SCLC) and non-small cell lung cancers (NSCLC).
• Staging of lung cancer refers to the extent to which the cancer has spread in the body.
• Treatment of lung cancer can involve a combination of surgery, chemotherapy, and radiation therapy as well as newer experimental methods.
• The general prognosis of lung cancer is poor, with overall survival rates of about 15% at 5 years.
• Smoking cessation is the most important measure that can prevent the development of lung cancer.

reference

Sugarbaker Oncology Associates Specialty Section for the Treatment of Peritoneal Mesothelioma

Peritoneal mesothelioma is a rare disease. The total number of cases per year in the United States is estimated between 100 and 500. A number of patients have a history of asbestos exposure. Because of the frequent dissemination of pleural mesothelioma to the peritoneal cavity, one must rule out spread from a primary pleural malignancy as the cause of peritoneal disease. No genetic, dietary, employment or geographic associations have been reported.

Peritoneal mesothelioma is unusual in that it demonstrates a wide spectrum of biological aggressiveness. The cystic variant of mesothelioma may cause recurrent episodes of severe lower abdominal pain but may not result in the death of the patient for many years. In contrast, the most aggressive mesothelioma variants may show metastases from the peritoneal surface to mesenteric lymph nodes at the time of initial surgery. Patients are diagnosed as having a malignant mesothelioma by histologic and immunocytochemical study. Frequent mitoses and increased size of the nucleus indicate an aggressive malignant process. Dissemination by cancer seeding and peritoneal fluid production would result in disease progression. As the peritoneal fluid produced by mesothelial nodules increased, dissemination to sites of peritoneal fluid resorption would be expected. Patients who are diagnosed with peritoneal mesothelioma often present to their physician with a large volume of ascites.

The widespread progression of malignant cells on peritoneal surfaces results in copious fluid production. The fluid production can be attributed to the retention of a functional property of normal mesothelial cells. In these patients the peritoneal space becomes a free conduit for mesothelioma cells to migrate from place to place. In the production of ascites fluid, the cancer cells provide themselves with a carrier solution to disseminate throughout the abdominal and pelvic spaces.

Treatment of Peritoneal Mesothelioma

Due to a lack of symptoms early in the natural history of peritoneal mesothelioma, a large majority of patients are first diagnosed with a large volume of disease diffusely spread throughout the abdomen and pelvis. The disease accumulates in largest volume at sites of peritoneal fluid reabsorption and at dependent sites by gravity. The small bowel surfaces and mesenteries are not spared of mesothelioma implants as in the mucinous appendiceal neoplasms.

Promising results of treatment from a new strategy: cytoreductive surgery plus perioperative intraperitoneal chemotherapy: Four groups have now reported on approximately 300 malignant peritoneal mesothelioma patients. The National Cancer Institute in Bethesda, MD, The Washington Cancer Institute in Washington, DC, The Columbia Mesothelioma Center in New York and the National Cancer Institute in Milan, Italy. Each group has reported their experience with between 50 and 100 patients. With current treatment all the groups report a median survival of 5 years or better. The median survival in the past was approximately 1 year (see Tables 1 and 2). As a result of this apparent major improvement in survival with a new treatment strategy, it has become standard of care for these patients.

1. Concerning neoadjuvant chemotherapy: A possible first treatment following diagnosis of peritoneal mesothelioma is systemic chemotherapy with Pemetrexed and cisplatin chemotherapy. This protocol was initiated at the National Cancer Institute of Italy and was not considered to be of benefit to these patients. However, anecdotal and beneficial responses have been noted. This chemotherapy which has approximately a 30% response rate may be of more value in an adjuvant setting after maximal mechanical and chemotherapy cytoreduction of the peritoneal mesothelioma has occurred. Neoadjuvant systemic chemotherapy was thought appropriate for biphasic or sarcomatoid malignant peritoneal mesothelioma.

2. Concerning the selection of patients using histological type of mesothelioma: All groups agree that the patients with sarcomatoid or biphasic peritoneal mesothelioma do not show great benefit from this treatment. Dr. Chabot and the Columbia Mesothelioma Center agreed with the limited benefits but advocated continued aggressive approach with patients found to have biphasic mesothelioma. The Washington Hospital Center group also suggested that patients with grade IV findings in the nucleus demonstrate a poor outcome with combined treatment. They suggested that these patients should also have neoadjuvant chemotherapy prior to initiating the combined approach. In those patients who show reduction in the volume of disease and symptomatic improvement, cytoreductive surgery with perioperative intraperitoneal chemotherapy may be considered. In those patients who do not have a response to first-line chemotherapy, then second-line chemotherapy with Gemzar can be recommended. In patients not responsive to either of these systemic chemotherapy treatments, best palliative care would be offered.

3. Regarding cytoreductive surgery: Cytoreductive surgery with peritonectomy is the first step in treatment of all four institutions. However, the extent of surgery varies considerably between the four groups. Perhaps the most conservative initial effort is proposed by Dr. Chabot. His initial treatment is a minimal debulking, usually only a greater omentectomy and removal of large tumor nodules. Then intraperitoneal ports are placed and the patient receives interval intraperitoneal chemotherapy using doxorubicin and cisplatin or mitomycin C and cisplatin. In his new protocol, heated intraperitoneal chemotherapy will be used at this initial event.

Dr. Pingpank at the National Cancer Institute, USA, advocated a visceral sparing cytoreduction. In this approach large cancer nodules would be removed, peritonectomy would be performed, however, complete removal of the disease would not be attempted.

At the National Cancer Institute of Italy and at the Washington Hospital Center, complete cytoreduction has been attempted down to no visible evidence of disease. Peritonectomy procedures of the right and left hemidiaphragm and pelvis are standard of care in this group of patients. Also, visceral resections of the right colon or left colon, if it leads to a substantial reduction in the volume of disease, is advocated.

The morbidity and mortality of the combined treatment is thought to be acceptable at dedicated treatment centers (Table 3).

4. Regarding the perioperative intraperitoneal chemotherapy: All groups advocated a cisplatin-based hyperthermic intraperitoneal chemotherapy. The doses were different at all four institutions. The heat, approximately 42.5ºC, was the same at all institutions. The drugs combined with cisplatin were doxorubicin and mitomycin C. At the National Cancer Institute, USA, high-dose cisplatin with systemic thiosulfate has been used.

5. Regarding early postoperative intraperitoneal chemotherapy: Two groups advocate taxol (Washington Cancer Institute) or taxol plus 5-fluorouracil (Naitonal Cancer Institute, USA) in the early postoperative period with a long dwell time of these drugs. At the National Cancer Institute, 125 mg/m² of paclitaxel and 800 mg/m² of 5-fluorouracil is given as a single instillation. At the Washington Cancer Institute, 20 mg/m²/day x 5 days (100 mg/m²) of paclitaxel is utilized.

6. Regarding interval chemotherapy: The Columbia Mesothelioma Center uses multiple cycles over a 6-month time period of intraperitoneal cisplatin plus doxorubicin or cisplatin plus mitomycin C. The Washington Cancer Institute uses multiple cycles of intraperitoneal paclitaxel with systemic cisplatin (bidirectional chemotherapy) for treatment of these patients. Currently, treatment plans utilizing intraperitoneal Pemetrexed and systemic cisplatin are being initiated as several institutions. The success with bidirectional (intravenous and intraperitoneal) chemotherapy that has been recently reported for patients with ovarian cancer should be directly applicable to peritoneal mesothelioma patients.

The role of systemic chemotherapy with Pemetrexed and cisplatin has yet to be determined after combined treatment. Currently, it is often used in this group of patients, especially those with aggressive disease and a suboptimal cytoreduction.

7. Regarding interval or symptomatic second-look surgery: At the Washington Cancer Institute a symptomatic second-look is used in patients at the first evidence of recurrence. With the symptomatic second-look, heated intraperitoneal chemotherapy is again used. A change in the chemotherapy solution should be considered. The results of treatment of patients using either interval or symptomatic second-look were thought to be improved.

8. Regarding follow-up and identification of patients with recurrent disease for possible symptomatic second-look: The CA-125 tumor biomarker is suggested as a follow-up for these patients. The progressive rise of CA-125 was identified as a signal of recurrent disease by the National Cancer Institute of Italy. CT scan with oral and intravenous contrast is a valuable follow-up tool in this group of patients. MRI is not thought to be of value. PET scanning is suggested as a new tool to be studied in this group of patients. PET scans may be most valuable when the readings move from negative to positive: this should strongly suggest progressive disease. Reoperation for low-volume disease is considered a potential part of the standard of care clinical pathway.

9. Regarding the use of intraperitoneal chemotherapy to palliate large-volume ascites: All agreed that patients with debilitating ascites from peritoneal mesothelioma respond well to debulking surgery plus the heated intraperitoneal chemotherapy. This use of the mechanical and chemical cytoreduction could be considered a standard of care for palliative management of patients with debilitating ascites.

Table 1. Median survival of diffuse malignant peritoneal mesothelioma using traditional treatment modalities (combined pleural and peritoneal mesothelioma*).

Authors	Year	No. of patients	Median Survival (months)
Chailleux et al.	1988	11/167	10*
Antman et al.	1988	37/180	15*
Sridhar et al.	1992	13/50	9.5*
Markman et al.	1992	19	9
Yates et al.	1997	14/272	14*
Neumann et al.	1999	74	12
Eltabbakh et al.	1999	15	12.5

Table 2. Results of treatment of cytoreductive surgery combined with perioperative intraperitoneal chemotherapy for diffuse malignant peritoneal mesothelioma (NA: median survival was not reached).

Chief Investigator	n -	Median survival (months)	Survival rates (%)
			1-year	2-year	3-year	5-year	7-year
Sugarbaker	100	52	78	64	55	46	39
Alexander	49	92	86	77	59	59	-
Deraco	49	NA	88	74	65	57	-
Glehen	15	36	69	58	43	29	-
Loggie	12	34	60	60	50	33	33
Morris	15	NA	76	63	63	-	-

Table 3. Morbidity and mortality of cytoreductive surgery combined with perioperative intraperitoneal chemotherapy for peritoneal mesothelioma.

Chief Investigator	n -	Morb (%)	Hem toxicity (%)	Blood loss (cc)	Op duration (hours)	Reoperation (%)	Mortality (%)	Hospital stay (days)
Sugarbaker	70	36	8	590	8.0*	11	3	23*
Alexander	49	25	26	-	6.5*	4	0	-
Deraco	49	27	-	-	-	-	0	-
Glehen	15	40	-	-	-	-	0	16
Loggie	12	-	-	-	-	-	8	-
Morris	15	36	-	-	9.6*	7	7	23*

Figure 1. Clinical pathway for diffuse malignant peritoneal mesothelioma.

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