IBS and Rectal Bleeding Causes

Can IBS cause bloody stools?

IBS and blood in stool, should I be worried?

When should you worry about rectal bleeding?

IBS and Rectal Bleeding

IBS blood in stool and mucus

Bloating and blood in stool

IBS blood when wiping

IBS rectal pressure

Can IBS cause bloody stools?

IBS can be a concerning and life disrupting digestive issue.

Many who have been diagnosed with IBS have a wide range of bowel related symptoms such as:

• Bloating
• Cramping
• Abdominal pain
• Constipation
• Diarrhoea

In many cases, the diagnosis of IBS is reached once other digestive problems have been excluded.  

This would often include examinations and tests for:

• Coeliac disease
• Lactose intolerance
• Inflammatory bowel diseases
• Bowel cancer/colon cancer
• Ovarian cancer

However, over time IBS symptoms can change and if blood is visible in the stool further investigations may be required to ensure not changes have taken place in the bowel. (1)

IBS and blood in stool, should I be worried?

Due to the nature of IBS, symptoms can change over time, with factors such as stress, medication and diet playing a role.

Rectal bleeding can be common in those with IBS-C, the type of IBS with constipation.   It’s often caused by small tears in the anus due to fecal impaction.  This is the increased load of feces (poo) in the rectum that places pressure on the lining that can then lead to injury.

This would commonly be seen in the stool a bright red blood due to the fact that it is reasonably fresh.  Typically, this would be noticed in small amounts on toilet paper.
However, if there is a sudden change in IBS symptoms and persistent blood in the stool lasting for several days, this would require further investigation from a doctor or gastroenterologist to rule anything else out.  In particular colon cancer which has better treatment outcomes if diagnosed at an early stage. (2)

When should you worry about rectal bleeding?

If symptoms of IBS change suddenly, particularly the frequency of bowel movements and increased pain and is accompanied by an increase amount of blood, further examination would generally be advised.

The shade and volume of the blood can also indicate the degree of concern.

Typically, if the individual is constipated and the blood that is present is bright red and in small amounts this is likely due to a small tear in the anus of haemorrhoids.

The appearance of blood in the stool can also take another form which may be harder to spot.

It is generally accepted that the further the blood travels through the colon, the darker it appears.  This means that can blood can appear in the stool in what can be described as “coffee grounds” and would take the appearance of dark spots in the stool which can indicate a bleed higher up within the digestive tract.

This may also lead to a stool that is generally darker in colour.

While this may indicate the need for further examination to rule out colon cancer.  Other causes of this are a tear, inflammation or certain medications.
NSAIDs (non-steroidal anti-inflammatory) medication such as Ibuprofen, in particular may contribute to irritation that can result in a bleed. (3)

IBS and Rectal Bleeding

While in severe cases of IBS, there may be blood, it is not a commonly experienced symptom.

IBS may be causes by infections in the digestive tract or as the consequence of viral of bacterial gastroenteritis.  In the acute period of these infections, bloody diarrhoea is not uncommon.  This would generally revolve once the infection has been cleared.
In some individuals, general symptoms of IBS may remain and be termed post infectious IBS (PI-IBS) however, even following the infection, blood would not be common. (4)

IBS blood in stool and mucus

The digestive tract has a thin layer of protective mucus covering its surface.  This may shed on a daily basis should not be visible in the stool.

However, when the lining of the digestive tract becomes inflamed or irritated, mucus production is increased to protect it.

This higher amount of mucus can often be visible in the stool of those with IBS and would be pale or white in colour.   
However, if there is a sudden increase in the amount of mucus produced alongside an increase in pain and the presence of blood, further investigation would often be suggested to investigate other causes such as colon cancer. (5)

Bloating and blood in stool

Bloating is one of the most common digestive symptoms and is present across a wide ride of gut conditions. 

These include:

• IBS
• SIBO
• Inflammatory bowel disease
• Coeliac disease
• Ovarian cancer 
• Colon cancer 

Due to its association with these other conditions, if bloating persist or worsens, further investigation can often be important to rule out any other conditions.
This would be particularly true if blood is present in the stool. (6)

IBS blood when wiping

Bright red blood that appears on toilet paper can often be a sign of a tear in the lining of the rectum.  Often the results of constipation or haemorrhoids.  

Dietary approaches to improving bowel movements can often ensure adequate fibre intake as well as maintaining optimal hydration.  
These 2 key factors to support bowel motility be help reduce fecal impaction reduce the strain placed on the bowel wall. (7)

IBS rectal pressure

This increase in rectal pressure in the bowel will not only be putting additional strain on the bowel wall but it may lead to changes in the balance on the beneficial bacteria in the colon.

This may be associated with an increase in methane producing organisms, who can then contribute to a further reduction in bowel motility and disruption within in the colon. (8)

References

1. https://www.ncbi.nlm.nih.gov/books/NBK534810/
2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1266237/
3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1239576/
4. https://www.fairview.org/patient-education/89211
5. https://www. ncbi.nlm.nih.gov/pmc/articles/PMC3758667/
6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3264926/
7. https://www.ncbi.nlm.nih.gov/books/NBK563143/
8. https://www.ncbi.nlm.nih.gov/books/NBK563143/

Changes You Should Not Ignore if You Have IBS

The symptoms of irritable bowel syndrome (IBS) can be difficult to manage. Flares or episodes are common in IBS which can cause a sudden worsening of symptoms or illness. Often, flares will occur even after you have been diagnosed and are on a treatment plan. This can be discouraging and lead to concerns that IBS has left you vulnerable to other conditions. However, this is not true. IBS is not a precursor to inflammatory or other gastrointestinal (GI) conditions. It does not increase your risk of developing gastrointestinal (GI) cancer. 

Learn more about the symptoms of IBS

Despite this, there are times when it may be best for your healthcare provider to review your symptoms and how they affect you. Here are suggestions for when to seek additional guidance from a medical professional.

Developments of Concern

Wrong beliefs about IBS may lead to distress, more healthcare provider visits, and unneeded tests. It helps to know, IBS:

• Does not cause physical damage
  • Does not increase the risk of colon cancer, inflammatory bowel disease (IBD), diverticulitis, or other gut disorders

On the other hand, IBS does not protect you from acquiring another disorder or condition. It also can coexist with another disorder.

Two situations provide alerts that another disease might be present:

• The presence of an “alarm” symptom or sign
• Clinical or family history linked to increased personal risk

Alarm Symptoms – “Alarm” signs and symptoms are commonly called “red flags.” “Alarm” signs simply identify changes which are neither explained by nor consistent with a diagnosis of IBS. These require additional review by a healthcare provider. “Alarm” symptoms may be a sign of an underlying disease that physically damages the gut but may also be related to other conditions.

For example, rectal bleeding is one of the most alarming of such symptoms. This may be due to a hemorrhoid or small tear (fissure) in the anal canal. Bleeding through the rectum can also imply unhealthy changes or damage to the gut wall that should not be ignored. Sometimes it could be due to inflammation, a large polyp, or tumor which requires treatment. Large amounts of red blood or black, tarry stool calls for urgent medical attention. Tarry stool refers to stool the color of tar which is caused by bleeding in the upper GI tract. 

There is a collection of symptoms that healthcare providers use to make sure something other than IBS is not causing symptoms. They are often called “Alarm signs” or “Alarm Symptoms”. These features include:

• New symptom onset at age of 50 or older
• Blood in the stools (red blood or black, tarry stool)
• Fever, shaking chills, or night sweats
• Nighttime symptoms that wake you up
• Unintentional weight loss
• Change in your typical IBS symptoms (like new and different pain)
• Recent use of antibiotics
• Family history of other GI diseases, like cancer, inflammatory bowel disease, or celiac disease

Learn more about alarm symptoms

Increased Personal Risk – Sometimes there is a factor in your life that may put you at greater than average risk of acquiring a serious intestinal disease. –Sometimes there are factors in your life that may put you at greater than average risk of developing an intestinal illness. Such examples are:

• Family history of chronic GI illness including cancer, Celiac, or IBD
• Sick contacts (e.g. family, friends, or co-workers) with recent intestinal illness
• Recent Travel: An infection may be suspected if you have recently traveled, had contact with others who are sick, or were possibly exposed to polluted water or food. Travel to the tropics or a developing country is a travel related risk factor.
• Antibiotic Use: Recent use of antibiotics or long hospital stays may increase the risk of an infection called C difficile. This infection typically appears with increasing abdominal pain and/or episodes of diarrhea (bloody or non bloody), nausea and/or vomiting. Sometimes fevers, chills, and sweats will occur as well. 

IBS patients are as likely as anyone to suffer an intestinal infection, which may add to and confuse the symptoms. You should be suspicious of an infection if:

• You have been traveling to tropical or developing parts of the world
• Friends and family are infected
• You have been exposed to possibly contaminated drinking water

Let your healthcare provider know about any of these concerns.

When to See your Healthcare Provider

IBS symptoms may be very hard to predict at first; however, over time most people become familiar with their symptoms. There may be intervals of relative calm, combined with periods of pain or discomfort. The flares may include chaotic bowel habits that interfere with daily life. However, the basic pattern of your symptoms should remain relatively stable.

If one of the previously described situations occurs or an alarm sign or new symptom emerges, it is time to see your healthcare provider. This allows them to decide if further testing or adjustments to your current IBS treatment is necessary. Sometimes a new drug or supplement may cause changes in symptoms. This is true even if they are not being taken for IBS. A change in your diet may also cause symptom changes, and your healthcare provider can help you make that determination.

Learn more about working with your healthcare provider

Putting it all Together

IBS is long-term (chronic) and tends to repeatedly come and go over time. It does not predispose you to other GI diseases. However, IBS does not protect you from other digestive conditions, and overlap is possible. New and different symptoms may make you suspicious that something new is happening.

You should visit your healthcare provider if you become aware of alarm symptoms or of a factor that might put you more than normally at risk of another disease. Your healthcare provider may review your symptoms and determine if further testing or treatment is necessary.

Usually, if the original diagnosis was sound, recurrent, but similar symptoms do not signify a new disease.

Adapted from IFFGD Publication: Changes You Should Not Ignore if You Have IBS Updated by: Walter Chan, MD, MPH, Director, Center for Gastrointestinal Motility, Assistant Professor, Harvard Medical School, Gastroenterology, Hepatology and Endoscopy, Boston, MA; Adapted from: W. Grant Thompson MD, FRCPC, FACG, Professor Emeritus, Faculty of Medicine, University of Ottawa, Ontario, Canada; Edited by: Darren Brenner, MD, Associate Professor of Medicine and Surgery, Northwestern University – Feinberg School of Medicine, Chicago, IL

Ischemic heart disease and anemia | Kirichenko A.A., Shatalova N.O., Grishin G.P., Fadeev A.M.

Coronary heart disease (CHD) is a pathology based on myocardial damage caused by insufficient blood supply. Atherosclerotic narrowing of the coronary arteries is the pathogenetic basis of coronary artery disease, but the development of myocardial ischemia requires an additional factor leading to an imbalance in the throughput of the coronary arteries and myocardial oxygen demand.

Most often, this is an increase in the work of the left ventricle (tachycardia, increased systolic blood pressure) or insufficiency of coronary blood flow (thrombus formation in the coronary arteries, spasm). Less often, as factors contributing to the development or progression of IHD, a decrease in perfusion pressure (DBP) or a violation of the oxygen transport function of the blood, etc.

are considered.
For clarity, we present extracts from the case histories of patients in whom these factors played the role of a “triggering mechanism”. The opinion that it is customary to wear pants only for men, and women should be sophisticated and elegant, preferring skirts and dresses, is absolutely not relevant at the present time.

Clinical case 1

Patient Sh., 84 years old, was hospitalized in May 2013 with complaints of pressing pain behind the sternum with little physical exertion and at rest.

For more than 30 years, high blood pressure numbers (up to 200/120 mm Hg), type 2 diabetes mellitus have been recorded.

4 months ago suffered an acute myocardial infarction without a Q wave of the lateral wall of the left ventricle. With coronary angiography: the anterior interventricular branch (ALV) of the left coronary artery (LCA) was stenotic in the proximal third by 50%, in the distal third — successive stenoses of 30–50%; the circumflex artery (OA) is stenotic in the middle third by 70%, the right coronary artery (RCA) is suboccluded in the anterior third, occluded in the middle third, the distal part is poorly contrasted by inter- and intra-arterial anastomoses. Stenting of the middle third of the OA was performed. RCA recanalization failed.

Attention was drawn to the presence of mild hypochromic anemia (hemoglobin -106 g/l). An examination of a possible source of bleeding did not reveal. He was discharged in a satisfactory condition with a recommendation to take acetylsalicylic acid and clopidogrel, hypoglycemic therapy, and iron supplements.

At home, he took the recommended drugs irregularly, did not visit the doctor.

About 2 months ago noted an increase in weakness. Rare bouts of retrosternal pain began to bother me. On the ECG dated May 10, 2013: against the background of sinus rhythm with a heart rate of 75 bpm, there is a pronounced depression of the ST segment in leads V2-6 (Fig. 1). He refused the offered hospitalization.

Last 2 weeks attacks of retrosternal pain of a pressing nature became more frequent, they began to occur with minimal physical exertion and at rest, sublingual nitroglycerin had a short-term effect, a feeling of lack of air appeared. He turned to the clinic, from where he was taken to the Central Clinical Hospital with a diagnosis of coronary artery disease, progressive angina pectoris.

On admission: pale skin. There are no edema. BH – 18 in 1 min. Breathing is hard. Pulse – 72, BP – 140/70 mm Hg. Art. on both hands. Systolic murmur at Botkin’s point and at the apex, conducted to the left axillary region.

ECG at admission (Fig. 2): sinus rhythm with a heart rate of 59 bpm, atrioventricular conduction delay (PQ – 0.24 s). Slow conduction in the left atrium and ventricle. Left ventricular hypertrophy. Violation of repolarization in V2-5.

EchoCG: LV myocardial hypertrophy (LVML – 240 g). Thickening of the interventricular septum (IVS), more pronounced in the basal part (1.6–1.8 cm), without signs of LV outflow obstruction. The thickness of the LVW is 1.5 cm. The contractility of the LV myocardium is satisfactory (EF according to Teicholz is 63%), the CSR is 3.6 cm, the CDR is 5.5 cm, the LA is 5. 1 cm. No zones of impaired kinetics were identified. Change in LV diastolic function of the first type.

Coronary angiography (CAG) was urgently performed (Fig. 3): the LCA trunk was not changed. The LAD is stenotic at the border of the anterior and middle thirds by 50%, along the distal third there are successive stenoses of 30–60%. 1DV — anatomically small, stenotic at the mouth by 80%, occluded in the middle third, the distal part is poorly contrasted by interarterial collaterals. VTK is stenotic at the mouth up to 50%. OV is anatomically large, passable throughout, previously implanted stents are without stenotic changes. The RCA is suboccluded in the anterior third, occluded in the middle third, the distal part is poorly contrasted by inter- and intra-arterial anastomoses. Balanced type of coronary blood supply.

Given the lack of dynamics of coronary artery stenoses compared to CAG in January 2013, percutaneous coronary intervention was not performed.

In the blood test: hemoglobin – 61 g / l, erythrocytes – 2. 30 × 10 * 12, CP – 0.8, hematocrit – 18.5, leukocytes – 7.7 × 10 * 9.

Cardiospecific enzymes (CPK MB, troponin T) were within the reference values.

In the analysis of urine: specific gravity – 1020, protein – 0.15, leukocytes – 0-5 in the field of view, erythrocytes – 100-150 in the field of view.

An additional targeted questioning made it possible to find out that over the past 4 months. there were repeated episodes of dark red urine, sometimes lasting for several days (gross hematuria?).

There was no convincing evidence of acute focal myocardial damage at the time of hospitalization. Given the presence of severe anemia, a transfusion of washed erythrocytes (1150 ml per 2 days) was performed with a positive effect: the hemoglobin level increased to 100 g/l, the number of erythrocytes – up to 3.59×10*12, hematocrit — up to 29.4.

On the ECG, 1 day after the last blood transfusion, normalization of the final part of the ventricular complexes in the chest leads is noted (in V4, the T wave is weakly negative).

The patient’s well-being improved significantly: over the next 3 days, with the expansion of the motor regimen to the level of physical activity corresponding to the 3rd functional class, there was no pain in the chest, the severity of dyspnea significantly decreased, the volume of loads was limited mainly by muscle fatigue. Episodes of gross hematuria did not recur. In a satisfactory condition, the patient was transferred for additional examination to the urological department.

Clinical case 2

Patient K., 50 years old, was hospitalized in December 2014 with progression of angina pectoris, dyspnea that occurs with minimal physical exertion, at rest, with an increase in general weakness during the last month.

Past medical history: AH with maximum known BP values ​​of 200/100 mm Hg. Art. more than 15 years old; regularly takes antihypertensive drugs, but blood pressure control is irregular. In 2002, he suffered an AMI, in the same year, coronary artery bypass grafting (CABG) was performed on the LAD, RCA, OA. In 2009the clinic of progressive angina pectoris developed, in connection with which the stenting of the shunt to the LCA was performed. In May 2014 – repeated AMI of the posterior wall of the left ventricle, systemic thrombolysis, percutaneous coronary intervention with recanalization and stenting of CABG to OA were performed. After discharge and until the present hospitalization, the patient’s condition is stable.

Concomitant diseases: type 2 diabetes mellitus, urolithiasis, chronic hemorrhoids, mild iron deficiency anemia has been recorded since 2009(did not take iron preparations).

On admission: the skin is pale, dry. BH – 18 beats / min. Breathing is hard, a small amount of wheezing on exhalation. Heart sounds are muffled. Heart rate -76 bpm. BP – 150/90 mm Hg. Art. on both hands.

The ECG was recorded against the background of a pain attack (Fig. 4): sinus rhythm, heart rate – 88 bpm, ST segment upward displacement from the isoline in leads III, aVF, V1. In leads I and aVL, the shift of the ST segment downwards from the isoline. Q wave lasting 0.04 s in II, III, aVF leads.

Echocardiography: LV myocardial hypertrophy (LVML – 213 g, IVS – 1.5 cm, ZSLV – 1.2 cm). Dilatation of the left atrium (5.3×6.1 cm). Violation of the diastolic function of the left ventricle of the first type. Hypokinesis of diaphragmatic, posterobasal and posterolateral segments. EF – 54% according to Teicholz.

In the general blood test: hemoglobin – 70 g / l, erythrocytes – 4.29 × 10 * 12, hematocrit -23.5, CP – 0.48, hypochromia, anisocytosis, poikilocytosis (ovalocytes, target erythrocytes), leukocytes – 5, 9×10*9. Serum iron – 1.9.

Cardiospecific enzymes (CPK MB, troponin T) were within the reference values.

Thus, there was no convincing evidence of acute focal myocardial damage at the time of hospitalization. It has been suggested that the cause of angina progression was severe iron deficiency anemia, most likely post-hemorrhagic. A transfusion of 630 ml of erythrocyte suspension was performed on the first day, parenteral administration of iron preparations was started.

Transfusion therapy was well tolerated. Anginal pain did not recur. On the ECG recorded after blood transfusion (Fig. 5): heart rate – 62 bpm. The ST segment returned to the isoline.

In the blood test after 1 day: the hemoglobin level increased to 105 g/l, the number of erythrocytes – up to 5.71 × 10 * 12, hematocrit – 38.3, CP – 0.55, hypochromia, anisocytosis persist. Leukocytes – 8 × 10 * 9.

For 3 days the patient was in the ICU, antianginal therapy was not required, because angina attacks did not recur.

A search for a possible source of blood loss was carried out, oncological search: colonoscopy revealed chronic combined hemorrhoids of the 3rd degree. No other pathology that could explain the presence of anemia was found.

A gradual expansion of the motor mode was carried out. Physical activity corresponding to the level of functional class 3 does not cause angina attacks and ECG signs of myocardial ischemia.

After 12 days in a stable condition, the patient was discharged for further treatment on an outpatient basis. The surgeon recommended the planned desarterization of hemorrhoids under ultrasound control.

Clinical case 3

Patient Z., 82 years old, was hospitalized with complaints of discomfort behind the sternum, lack of air, arising without a clear connection with physical activity, lasting up to 4-5 minutes, the day before there was a protracted attack lasting more than 1 hour, severe weakness, sweating. A real deterioration in the condition has been noted during the last 3 days against the background of hypotension that has appeared.

Within 2 weeks before hospitalization, he took non-steroidal anti-inflammatory drugs (NSAIDs) (ketorolac) for dorsalgia. 4 days ago, he noted the appearance of rapid liquid stools of dark color, unusually low blood pressure – 80/40 mm Hg. Art.

In 1995, he suffered an AMI of the inferior LV wall. In the same year, mammary-coronary bypass grafting of the LAD, CABG of the PBV OA and RCA was performed. In 2003 – linear aortofemoral bypass with a synthetic prosthesis on the left. The early postoperative period was complicated by the development of repeated AMI of the inferior LV wall.

Since 2009 – paroxysms of atrial tachyarrhythmia.

Constantly taking bisoprolol — 2.5 mg/day, perindopril — 5 mg/day, atorvastatin — 20 mg/day, warfarin — 5 mg/day. INR control was not carried out for more than a year.

On admission: the skin and visible mucous membranes are pale. The number of breaths is 20 per 1 min. Breathing is weak, hard. Heart sounds are deaf, rhythmic. Heart rate – 76 beats / min. BP – 110/70 mm Hg. Art.

Laboratory data: hemoglobin – 91 g / l, erythrocytes – 3.93 × 10 * 12, hematocrit – 33.0, CP – 0.84, leukocytes – 10.2–10.6 × 10 * 9, platelets – 223 × 10*9, anisocytosis, anisochromia.

Cardiospecific enzymes: CPK — 268 on admission, after 10 hours — 319, CPK MB – 30 at admission, after 10 hours – 42, troponin T at admission – 177, after 10 hours – 538.

Serum iron – 13 µmol, iron transport proteins within the normal range. Coagulogram: APTT – no coagulation, INR – no coagulation, fibrinogen – 3.3 g/l, D-dimer – 1147.

ECG (Fig. 6) on admission: sinus rhythm, stage 1 AV block, cicatricial changes in the inferior LV wall, ST segment shift in leads II, III and avF, high R in V1-2. ECG archive not provided.

Echocardiography: sclerosis and calcification of the aortic walls, annulus and cusps of the aortic valve. LVML – 204 g, IVS thickness – 1.0 cm, ZLV – 1.0 cm. Dilatation of the left heart (LA – 4.5 × 5.5 cm, left ventricle: ESR – 92, EDV – 171). Relative insufficiency of MK II degree. Hypokinesis of the middle posterior and posterolateral LV segments. Decreased global contractility of the LV myocardium (EF according to Teicholz – 47%). Diastolic dysfunction of the left ventricle of the first type.

Taking into account complaints, anamnesis, laboratory and instrumental data, the patient was diagnosed with repeated AMI of diaphragmatic and posterior basal localization.

Gastrointestinal bleeding that occurred while taking NSAIDs and an oral anticoagulant was not ruled out, in connection with which EGDS was urgently performed: endoscopic signs of chronic esophagitis, ulcer of the lower third of the esophagus Forrest II C. Acute gastric ulcer Forrest II B (without signs of ongoing bleeding). Pyloric ulcer Forrest I B (with signs of ongoing bleeding). After endoscopic injection hemostasis, the bleeding was stopped.

The cause of AMI was probably hypotension and anemia on the background of gastrointestinal bleeding. Started conservative hemostatic, antiulcer therapy. It was decided to refrain from performing CAG with possible percutaneous coronary intervention until the condition stabilizes.

During treatment, blood pressure figures stabilized at 120/85 mm Hg. Art., hemoglobin level increased to 110 g / l, the number of erythrocytes increased – up to 5.71 × 10 * 12, hematocrit – 38.3, CP – 0.55, leukocytes – 8 × 10 * 9, hypochromia, anisocytosis persist.

The level of CPK activity decreased to 113 units, CPK MV – to 12.7, troponin T – to 225.

Endoscopy after 2 days: ulcer of the lower third of the esophagus Forrest III, acute gastric ulcer Forrest III, pylorus ulcer Forrest II C (no signs of bleeding, appearance of fibrin in the bottom area).

On the 3rd day of stay in the hospital, short-term attacks of compressive pain behind the sternum resumed (2 attacks: during meals and when trying to sit up in bed).

According to urgent indications, coronary angiography was performed (Fig. 7): the LCA trunk was stenotic in the anterior and middle third up to 70%, suboccluded in the distal third with the transition to the mouths of the OB and LAD; The LAD is suboccluded at the orifice, 80% stenotic in the anterior third, occluded in the middle third, the distal part is contrasted by a functioning mammary-coronary bypass graft. OB is suboccluded at the mouth, stenotic in the anterior third by 80%; The RCA is suboccluded along the anterior and middle thirds, occluded at the border of the middle and distal thirds, the distal part is contrasted by interarterial anastomoses.

Right type of coronary blood supply.

The mammary-coronary bypass from the right mammary artery in the distal third of the LAD is passable. Shunts to OA and RCA are not visualized.

An attempt to recanalize stenotic arteries was unsuccessful due to severe calcification.

Over the next day, a state with negative dynamics: in the form of an increase in short-term angina attacks, accompanied by pronounced ECG signs of myocardial ischemia (Fig. 8). A decrease in hemoglobin from 110 to 87 g/l, hematocrit to 26.0 was noted.

Cardiospecific enzymes within normal limits. Echocardiography: the size of the left parts of the heart is the same, no new areas of LV wall motion disorder were detected.

Gastroscopy: active bleeding from an acute mucosal defect of the cardioesophageal junction (Forrest I). Endoscopic hemorrhage control.

After transfusion of 600 ml of erythrocyte suspension, a state with positive dynamics: anginal pain and ECG signs of myocardial ischemia do not recur (Fig. 9), restoration of the level of hemoglobin (110 g/l), erythrocytes (3.85×10*12), hematocrit -33.7.

With the control EGDS after 10 days, there was a positive trend – a decrease in the size of ulcerative defects without signs of bleeding.

On the background of therapy with proton pump inhibitors, β-blockers, clopidogrel 75 mg/day, the red blood counts are stable, the motor mode is expanded and corresponds to 3 FC in terms of the level of loads.

HMECG: sinus rhythm, heart rate (per day/day/night): 78/77/78 beats/min, maximum heart rate — 99 beats / min, minimum – 64 beats / min. The appearance of ST segment depression is noted with an increase in heart rate over 90 beats / min.

The above cases demonstrate the possibility of manifestation of coronary insufficiency against the background of a decrease in the oxygen-transporting capacity of the blood in both patients with severe and moderate lesions of the coronary bed. Elimination of anemia in all three cases contributed to an increase in coronary reserve and stabilization of the condition.

forms and risk factors for complications of IHD

Ischemic disease occupies a leading position among cardiovascular diseases that have severe consequences – disability and death. How the disease proceeds, what to do to reduce the risk of acute and chronic complications, and also for what symptoms you need to urgently call an “ambulance” – we tell in the article.

The course of the disease, its forms and complications

Classification IHD differs from the classifications of other diseases: since coronary disease itself is a state of imbalance between the supply of oxygenated blood to the myocardium and the need of the heart for it, it is difficult to draw an unambiguous line between its forms and complications. So, both myocardial infarction and heart failure are both clinical forms of the course of the disease (acute and chronic ), and complications caused by lack of myocardial oxygenation.

In this regard, the medical community speaks of the clinical classification of IHD forms in the following order:

• Sudden coronary death (cardiac arrest).

• Angina pectoris : exertional angina (new onset, stable, unstable or progressive) and rest angina (spontaneous/vasospastic/variant/Prinzmetal) are distinguished.

• Myocardial infarction.

• Postinfarction cardiosclerosis.

• Heart failure (acute and chronic).

• Violations of cardiac rhythm .

• Painless myocardial ischemia.

• hibernating myocardium.

• Stunned myocardium.

• X syndrome.

The development of the disease is not linear, and clinical forms can replace each other. If you do not follow the recommendations of the attending physician, chronic forms of IHD may be complicated by an acute form (heart attack or sudden coronary death). At the same time, after an acute form of coronary artery disease (the same heart attack), chronic consequences of ischemia develop in the form of postinfarction cardiosclerosis

Both acute and chronic forms of coronary artery disease can lead to severe consequences for the body.

Risk factors for the development of IHD complications

In a general sense, the risk factors for the development of IHD are not much different from the risk factors for heart failure and any other pathology of the heart and blood vessels of a non-infectious nature.

How to reduce the risk of complications

The simplest prevention of coronary disease is to maintain a healthy lifestyle: proper nutrition, adherence to the daily routine and the rejection of bad habits.

In a narrower sense, secondary prevention is very important, that is, compliance with the doctor’s instructions for an already diagnosed pathology. In addition to correcting behavioral risk factors, secondary prevention of coronary artery disease should include the following:

• Control of lipid metabolism. The basis of atherosclerotic changes in blood vessels is the deposition of lipid complexes in their walls, which leads to a progressive narrowing of the lumen of the arteries . The fight against the risk of complications includes lowering the level of total cholesterol, including medication. A level of up to 4.2-4.8 mmol / l is considered safe. With an increase in this indicator by 10 mg / dl, the risk of progression of stenosis arteries is growing by 1%.

• Blood pressure control. Hypertensive patients are at risk of developing coronary artery disease three to four times more than people with normal pressure. The risk of stroke in such patients increases seven times compared with normotonic people – people with normal blood pressure.

• Complete cessation of smoking. This bad habit increases the risk of developing angina, and is an important long-term risk factor for sudden cardiac death.

• Body weight control. Overweight and obesity predetermine the development of up to 17-23% of cases of CHD. At the same time, about 30% of obese people have disorders or other eating disorders, which requires a revision of the diet and correction of eating habits. However, there are also cases requiring medical intervention (endocrine and cerebral forms of obesity).

• Psycho-emotional stability of the patient. Exposure to strong emotions, including stress, leads to a sharp spasm of the coronary vessels, increasing the risk of myocardial infarction or sudden cardiac death.

The most effective prevention of the development of coronary artery disease and its complications is a healthy lifestyle.

IHD red flags: when to call a doctor

In a clinical sense, both acute and chronic forms coronary disease pose a danger to life. However, in the first case, hours and minutes count, so it is important to know for which symptoms you should immediately seek medical help.

Signs of acute myocardial ischemia:

• discomfort, pain or burning in the heart or behind the sternum;

• pain radiates to the left arm, left half of the lower jaw, neck, back or abdomen;

• attacks of pain last for 3-5 minutes and recur periodically.

These symptoms most often occur with angina pectoris , can be provoked by any physical activity, stress, cold, smoking and stop when the cause is eliminated or nitroglycerin is taken.

Important! Similar symptoms occur in the first minutes of myocardial infarction. A doctor should be called immediately if the pain does not stop within 15 minutes or after taking nitroglycerin or the dose of antianginal drugs recommended by the attending physician.

Urgently call an ambulance if:

• the pain repeats in waves even at rest, and its intensity increases;

• weakness appears, accompanied by fear;

• pulse and blood pressure fluctuate;

• there is sweating and a feeling of lack of air.