Pick’s Disease – Common Symptoms and Causes

Written by Rachel Reiff Ellis

• Causes
• Symptoms
• Pick’s Disease vs. Alzheimer’s Disease
• Diagnosis
• Treatment

Pick’s disease is a kind of dementia similar to Alzheimer’s but far less common. It affects parts of the brain that control emotions, behavior, personality, and language. It’s also a type of disorder known as frontotemporal dementia (FTD) or frontotemporal lobar degeneration (FTLD).

Your brain uses a transport system to help move around the nutrients it needs. This system is made of proteins that like railroad tracks guiding trains guide nutrients where they need to go. The proteins that keep the tracks straight are called tau proteins.

When you have Pick’s disease, the tau proteins don’t work the way they should. You may also have more of them in your brain than other people.

These abnormal clumps of tau proteins are called Pick bodies. Pick bodies “derail” your transport system. The track is no longer straight, and nutrients in the brain can’t get where they need to go. This causes brain damage that can’t be reversed.

Around 50,000 to 60,000 people in the U.S. have Pick’s disease. It’s usually diagnosed between the ages of 40 and 75, but it can happen in people as young as 20. It affects more men than women. People of Scandinavian descent are at a slightly higher risk of getting it than others.

Up to 25% of people with Pick’s disease received a gene that causes it from a parent. Experts aren’t sure why it happens in other cases.

Pick bodies typically form in the frontal and temporal lobes of the brain. These sections control your behavior, personality, and speech. Symptoms usually show up in those areas.

You may:

• Act aggressively toward others
• Be uninterested in everyday activities
• Be very aware of everything you do all the time
• Feel irritable or agitated
• Have drastic and quick mood swings
• Have trouble feeling warmth, sympathy, or concern for others
• Have trouble with unplanned activities
• Make rash decisions
• Repeat actions over and over
• Say and do inappropriate things

Some people become hungry all the time, and some develop an unhealthy “sweet tooth” and eat much more sugar than they should.

Problems with language usually happen early in the disease. Pick bodies in the speech section of your brain can cause problems with:

• Recalling names of common objects
• Copying simple shapes with pencil and paper
• Understanding written words
• Speaking because of halted or stilted speech

Occasionally, people with Pick’s disease might also have:

• Memory loss
• Problems moving
• Stiff or weak muscles
• Trouble peeing
• Trouble with coordination

Pick’s disease has many of the same causes and symptoms that Alzheimer’s does. But there are key differences.

Unlike people with Alzheimer’s disease, people with Pick’s disease:

• Are diagnosed earlier in life
• Don’t have hallucinations or delusions
• Don’t tend to get lost in familiar places
• Have a harder time making sense of their words or the words of others
• Have behavior problems early on (behavior problems usually come late in Alzheimer’s)
• Don’t have as many memory loss problems

To find out if you have Pick’s disease, your doctor will ask about your symptoms and go over your medical history. Then you’ll have special tests that check your memory, behavior, language, and other mental functions. These are usually pencil and paper tests. You’ll answer questions in writing and may be asked to draw certain objects.

The doctor may also recommend a blood test that looks at your DNA to see if you have the gene that causes Pick’s disease.

To get a better picture of what’s happening in your brain, your doctor may order imaging tests, such as:

• Magnetic resonance imaging (MRI): Powerful magnets and radio waves are used to make detailed images of your brain.
• Single-photon emission computed tomography (SPECT) or a positron emission tomography (PET) scan: A radioactive substance and a special camera create 3-dimensional pictures that show what areas of your brain are more or less active.

You may also have a lumbar puncture. Your doctor will use a long needle to take a small amount of fluid from an area near your spine for screening. In rare cases, your doctor might want to take a small amount of your brain tissue to test. This is called a biopsy.

There’s no cure for Pick’s disease, and medications can’t slow it down. It can progress slowly, but usually, it steadily gets worse over time. Some people live as long as 10 years with the disease.

Your doctor can recommend treatment to help you deal with many of your symptoms. They may suggest behavioral therapy to help control any dangerous behavior and antidepressants to help with agitation or aggression.

Top Picks

Pick Disease – StatPearls – NCBI Bookshelf

Continuing Education Activity

Pick disease, also known as frontotemporal dementia, is the most common cause of dementia in patients under 60 years of age and is the third most common cause of dementia in patients over 65 years old. This type of dementia is characterized by a spectrum of neuropsychiatric symptoms ranging from those that affect the patient’s personality to those that cause a decline in cognitive function. This activity reviews the evaluation and management of Pick disease and highlights the role of the interprofessional team in the care of patients with this condition.

Objectives:

• Identify the etiology and epidemiology of Pick disease.

• Review the appropriate history, physical, and evaluation of Pick disease.

• Outline the treatment and management options available for Pick disease.

• Summarize interprofessional team strategies for improving care coordination and communication to advance the care of Pick disease and improve outcomes.

Access free multiple choice questions on this topic.

Introduction

Frontotemporal dementia (FTD) is a progressive, neurodegenerative disorder characterized by behavioral changes and language deficits with frontal and temporal cortical degeneration. It is a heterogeneous condition featuring a variegated constellation of overlapping clinical, genetic, and pathological variables resulting in an individual phenotypic expression of disease. Often referred to as Pick’s disease, this dementia syndrome commonly occurs in pre-senile patients and is divided into behavioral variant (bvFTD) and primary progressive aphasia (PPA) subtypes. PPA is further categorized as nonfluent/agrammatic variant (nfvPPA), semantic variant (svPPA), and logopenic aphasia. Motor neuron disease (FTD-MND), progressive supranuclear palsy (PSP-S), and corticobasal syndrome (CBS) are overlapping syndromes falling within the spectrum of the frontotemporal diagnosis.[1]

The natural history of frontotemporal dementia is marked by an insidious onset followed by a steady decline from diagnosis to death characterized by a significant physical, mental, social, and financial burden for patients, families, and caregivers.

Etiology

Although the majority of frontotemporal dementia presentations are sporadic, the disease is highly heritable, and a family history of dementia has been reported in up to forty percent of cases. [2][3] Ten to twenty percent of patients feature genetic mutations with an autosomal dominant pattern of inheritance.[2][4] Three primary genes have been documented as agents of disease etiology, microtubule-associated protein tau (MAPT), progranulin (GRN), and C9orf72 with a number of other genes implicated with less frequency.[5][6] 

Few studies have evaluated modifiable risk factors for frontotemporal dementia; however, research has identified diabetes mellitus, history of head injury, and autoimmune disorders as potentially contributing to the development of frontotemporal dementia.[7] Hypertension, smoking, obesity, and a history of cerebrovascular accidents have also been analyzed.[7] More investigation is required to confirm these associations and formally recommend lifestyle modification to mitigate the risk of frontotemporal dementia.[7]

Epidemiology

Frontotemporal dementia is the second most common etiology of early-onset dementia in patients under 65 years of age constituting ten percent of pathologically confirmed cases. Three percent of dementias in patients of any age are attributable to frontotemporal disease.[5] While the condition manifests most often in the fifth and sixth decades of life, onset has been recorded in patients as young as their thirties and over seventy.[1][8]

The behavioral variant of frontotemporal dementia comprises sixty percent of cases with the primary progressive aphasia subtypes occurring less frequently. Estimates for prevalence and incidence are 15 to 22 per 100,000 and 2.7 to 4.1 per 100,000, respectively, with those statistics likely under-representing actual figures due to the diagnostic difficulties of frontotemporal dementia.[1][9] The United States and national numbers are similar; however, developing countries are poorly represented in most epidemiologic studies, and data on non-white populations is also lacking.[9] Studies have not revealed any differences in gender distribution.[9]

Pathophysiology

While the pathophysiology of Alzheimer’s dementia is well-established and consistent among cases, the mechanism behind frontotemporal dementia is heterogeneous and complex, requiring continued investigation amongst researchers. [10] Atrophy of the frontal and anterior temporal lobes secondary to intraneuronal deposition of abnormal protein inclusion bodies is the primary pathological focus. Tau, transactive response DNA binding protein 43 (TDP-43), and RNA-binding protein fused in sarcoma (FUS) have been identified as the principal proteins responsible for frontotemporal dementia.[11] They have been attributed to individual genetic mutations and are associated with the varying phenotypic expressions of the different frontotemporal dementia subsets.[11]

History and Physical

Initial presentations of frontotemporal dementia are individualized based on the disease variant being expressed; however, in later progression, there is a significant overlap between behavioral and language subsets. Being a mostly clinical diagnosis, a thorough history must be obtained from patients and families to confirm the disorder and delineate which variant is present. 

Symptoms of behavioral variant frontotemporal dementia (bvFTD) can be organized into six categories of behavioral or cognitive decline. Behavioral disinhibition featuring socially inappropriate behavior, loss of social decorum, or impulsive, careless actions are often observed. Apathy is common and is frequently misdiagnosed as depression. Loss of empathy or sympathy is characterized by a lack of interest or disregard for other’s feelings. Perseverative, stereotyped, or compulsive behaviors manifest as repetitive movements, compulsive and ritualistic routines, and stereotyped speech. Hyperorality and dietary changes can include binge eating, change in preference for sweets and alcohol, and pica with oral exploration. Executive dysfunction can occur, sparing loss of episodic memory and visuospatial skills characteristic of Alzheimer’s dementia. Deficits in three of these six diagnostic criteria are required for a definitive diagnosis of behavioral variant frontotemporal dementia (bvFTD).[1] 

The language variant of frontotemporal dementia known as primary progressive aphasia (PPA) is divided into three clinical syndromes, nonfluent/agrammatic primary progressive aphasia (nfvPPA), semantic variant primary progressive aphasia (svPPA), and logopenic aphasia.  Clinical criteria for nfvPPA include effortful speech, speech apraxia, and agrammatism. Object knowledge and single-word comprehension are unaffected; however, complex sentence understanding may be impaired. Semantic dementia features anomia and impaired single-word comprehension. Along with these classic findings, three of the following four phenomena must be present: impaired object knowledge, surface dyslexia, and dysgraphia, spared repetition, and no disruption of speech production. Patients with logopenic variant PPA exhibit word-finding difficulty and repetition of sentences and phrases. Phonological speech errors are displayed, while single-word comprehension, object knowledge, motor speech, and simple grammar are unaffected. As with all frontotemporal dementia presentations, language variants are heterogeneous, and later stages feature overlapping symptoms as neurodegenerative pathologies spread to varied cerebral structures.[1] 

Further overlap can be seen in frontotemporal dementia-related syndromes such as motor neuron disease, corticobasal degeneration, and progressive supranuclear palsy. The ALS-parkinsonism-dementia complex has been described and demonstrates the coexistence of these motor neuron pathologies with frontotemporal dementia. Corticobasal degeneration presents with asymmetric movement impairment, and progressive supranuclear palsy features supranuclear gaze palsy with postural instability and falls. These conditions can coincide with behavioral and language deficits found in frontotemporal dementia.[1]

Evaluation

Imaging and fluid biomarkers are the primary focus in current and future evaluations of frontotemporal dementia. Standard, structural magnetic resonance imaging (MRI), and computed tomography (CT) modalities can demonstrate characteristic atrophy of frontal and temporal lobe grey matter.[2] At the vanguard of frontotemporal dementia imaging applications are diffuse tensor imaging for evaluating white matter integrity loss, fluorodeoxyglucose positron emission tomography (FDG-PET) to monitor localized brain metabolism, amyloid and tau PET traces which detect cerebral protein deposition, arterial spin labeling (ASL) measuring regional perfusion, and resting-state functional MRI (RS-fMRI) analyzing functional connectivity between brain structures. [2][6] 

Further studies are necessary to implement these techniques in diagnosing frontotemporal dementia, isolating which disease subset is present, differentiating between other dementia syndromes such as Alzheimer’s, and longitudinal monitoring of disease progression. 

Cerebrospinal fluid and serum protein biomarkers are presently utilized to exclude Alzheimer’s disease in the assessment of frontotemporal dementia and are under appraisal for prospective diagnostic indications and monitoring pathologic progression and response to potential therapies. Elevated CSF tau proteins and decreased beta-amyloid 42 protein concentrations can accurately confirm Alzheimer’s dementia and are validated for eliminating frontotemporal dementia from the differential.[6]

Neurofilament light chain (NFL) proteins are increased in serum and CSF samples of patients with frontotemporal dementia and other neurodegenerative disorders and have promising applications in future frontotemporal dementia assays. [6] Gene-specific biomarkers such as progranulin and poly (GP) have the potential for investigating the expression of GRN and C9orf72 frontotemporal dementia mutations, respectively.[6] As with potential imaging techniques, more data is needed to implement fluid biomarkers into a comprehensive frontotemporal dementia evaluation strategy.

Treatment / Management

No current disease-modifying, curative therapies exist for frontotemporal dementia. Treatment must center upon symptom management with particular consideration for supportive measures for patients, families, and caregivers. There is a consensus that selective serotonin reuptake inhibitors (SSRIs) are beneficial in the management of behavioral symptoms.[1][12] Low-dose atypical antipsychotics may be implemented for aggressive or disruptive behaviors; however, caution must be advised due to black-box warning for cardiac events in the elderly.[3] Therapeutics for Alzheimer’s dementia, such as cholinesterase inhibitors, are ineffective and may precipitate behavioral abnormalities in frontotemporal dementia. [3] 

Non-pharmacologic interventions have a prominent role in addressing symptoms and delaying disease progression. Physical therapy and exercise can slow cognitive decline while speech therapy may mitigate language deficits in patients with the primary progressive aphasia variants.[1] With the functional decline, patients will require assistance with activities of daily living, and a safe home environment must be secured. Formulating non-pharmacologic behavioral management strategies and implementing them consistently may assuage the physical, mental, and social burden of patient misconduct.[12]

Patient and caregiver education is paramount and can ameliorate the guilt and stigma associated with the neuropsychiatric features of the disease. Support groups and community resources must be made available to caregivers, and their psychological health should be featured in family discussions.[13] A conservatorship can be established to address financial and legal distress associated with the condition. [12]

Differential Diagnosis

There are abundant symptom overlaps between frontotemporal dementia and other neuropsychological disorders. Psychiatric conditions such as depression, bipolar disorder, and, most significantly, schizophrenia can mimic behavioral variant frontotemporal dementia and are often misdiagnosed during early presentations of frontotemporal disease.[5] Onset and progression patterns can assist in differentiating schizophrenia from frontotemporal dementia. While frontotemporal dementia generally occurs in patients over forty-five years of age, initial presentations of schizophrenia are observed in younger age groups.[5] A consistently advancing disease course characterizes frontotemporal dementia, while schizophrenia progression is variable and can plateau.[5] 

Distinguishing other dementia syndromes from frontotemporal dementia can also be challenging. A predominance of memory and visuospatial deficits suggests the more prevalent Alzheimer’s dementia variant. Lewy body dementia should be considered in the setting of visual hallucinations and parkinsonism.[8] 

Several miscellaneous conditions can present with neuropsychiatric and behavioral symptoms similar to frontotemporal dementia including, infections, toxins, neoplasms, trauma, paraneoplastic disease, autoimmune disorders, thyroid syndromes, hepatic encephalopathy, and various genetic pathologies.[8]

Prognosis

The heterogeneous nature of frontotemporal dementia, as well as its relatively low prevalence compared to Alzheimer’s disease, has led to difficulty defining accurate prognosis and life-expectancy figures. Survival rates feature a wide distribution depending on the subset of phenotypes being evaluated. Patients with the motor neuron disease variant have the shortest disease course at two to three years from diagnosis to death.[9] The median life expectancy for behavioral variant frontotemporal dementia is nine years, while patients with semantic dementia have survival rates of twelve years, comparable to the generally slower progression of Alzheimer’s dementia. [3][9]

Complications

The functional and cognitive decline associated with frontotemporal dementia spawn predictable somatic, psychological, and social complications for patients and their caregivers. Dysphagia is likely responsible for the increased incidence of pneumonia and respiratory failure, a significant cause of mortality in frontotemporal dementia.[13] Sequelae of swallowing difficulties include weight loss, protein-calorie malnutrition, and subsequent failure to thrive.[13][14] 

Cardiac disease, attributed to patient’s sedentary and bedridden immobility status, is implicated in the most significant number of frontotemporal dementia deaths.[13][14] Gait disturbances precipitate an increased risk of falls and traumatic injury.[13]

Consultations

Consultations with neurology and psychiatry are fundamental to the management of frontotemporal dementia. Geneticist evaluation may be indicated in patients with a significant family history of neurologic disorders. An interprofessional approach featuring physical and occupational therapists, dieticians, and support groups provide the comprehensive care required for patient and caregiver’s physical and emotional health.[3] Palliative specialists can allay the burden for individuals and their families experiencing end-of-life transitions.[14]

Deterrence and Patient Education

Patient and caregiver education should be at the forefront of frontotemporal dementia management plans. Information regarding the disease process and progression, especially the behavioral components, can alleviate social stress and guilt associated with potential, perceived patient misconduct. Preparing families and caregivers for the physical, psychological, social, and financial toll that may follow the diagnosis can stabilize the care environment and promote the overall effectiveness of the care team.

Enhancing Healthcare Team Outcomes

The heterogeneous nature of frontotemporal dementia, along with its insidious onset, precipitous decline pattern, and substantial impact on patients’ and caregiver’s lives necessitates a comprehensive diagnostic, management, and educational care plan. Interprofessional cooperation and communication are imperative to shape a capable healthcare team and to minimize the physical, mental, and emotional burden of the disorder. A patient-centered medical home model comprised of a primary clinician coordinating care between neurologists, psychiatrists, geneticists, physical, occupational, and speech therapists, dieticians, nurses, home health workers, palliative specialists, support groups, and community resources are essential to improving the quality of life of all involved. [Level 5]

The exponentially increased emphasis on frontotemporal dementia genetic and molecular pathologies research over the last several years has led to hopeful optimism for new, targeted, disease-modifying therapies, imaging technologies, and chemical biomarkers to expand our armamentarium to combat frontotemporal dementia. [Level 5]

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References

1.

Olney NT, Spina S, Miller BL. Frontotemporal Dementia. Neurol Clin. 2017 May;35(2):339-374. [PMC free article: PMC5472209] [PubMed: 28410663]

2.

Kelley RE, El-Khoury R. Frontotemporal Dementia. Neurol Clin. 2016 Feb;34(1):171-81. [PMC free article: PMC5549462] [PubMed: 26613998]

3.

Bang J, Spina S, Miller BL. Frontotemporal dementia. Lancet. 2015 Oct 24;386(10004):1672-82. [PMC free article: PMC5970949] [PubMed: 26595641]

4.

Devenney EM, Ahmed RM, Hodges JR. Frontotemporal dementia. Handb Clin Neurol. 2019;167:279-299. [PubMed: 31753137]

5.

Cipriani G, Danti S, Nuti A, Di Fiorino M, Cammisuli DM. Is that schizophrenia or frontotemporal dementia? Supporting clinicians in making the right diagnosis. Acta Neurol Belg. 2020 Aug;120(4):799-804. [PubMed: 32314269]

6.

Meeter LH, Kaat LD, Rohrer JD, van Swieten JC. Imaging and fluid biomarkers in frontotemporal dementia. Nat Rev Neurol. 2017 Jul;13(7):406-419. [PubMed: 28621768]

7.

Rasmussen H, Stordal E, Rosness TA. Risk factors for frontotemporal dementia. Tidsskr Nor Laegeforen. 2018 Sep 18;138(14) [PubMed: 30234270]

8.

Rosness TA, Engedal K, Chemali Z. Frontotemporal Dementia: An Updated Clinician’s Guide. J Geriatr Psychiatry Neurol. 2016 Sep;29(5):271-80. [PubMed: 27502302]

9.

Onyike CU, Diehl-Schmid J. The epidemiology of frontotemporal dementia. Int Rev Psychiatry. 2013 Apr;25(2):130-7. [PMC free article: PMC3932112] [PubMed: 23611343]

10.

Hodges JR, Piguet O. Progress and Challenges in Frontotemporal Dementia Research: A 20-Year Review. J Alzheimers Dis. 2018;62(3):1467-1480. [PMC free article: PMC5870022] [PubMed: 29504536]

11.

Haass C, Neumann M. Frontotemporal dementia: from molecular mechanisms to therapy. J Neurochem. 2016 Aug;138 Suppl 1:3-5. [PubMed: 27502123]

12.

Cardarelli R, Kertesz A, Knebl JA. Frontotemporal dementia: a review for primary care physicians. Am Fam Physician. 2010 Dec 01;82(11):1372-7. [PubMed: 21121521]

13.

Caceres BA, Frank MO, Jun J, Martelly MT, Sadarangani T, de Sales PC. Family caregivers of patients with frontotemporal dementia: An integrative review. Int J Nurs Stud. 2016 Mar;55:71-84. [PubMed: 26612696]

14.

Diehl-Schmid J, Richard-Devantoy S, Grimmer T, Förstl H, Jox R. Behavioral variant frontotemporal dementia: advanced disease stages and death. A step to palliative care. Int J Geriatr Psychiatry. 2017 Aug;32(8):876-881. [PubMed: 27374872]

Disclosure: Micah Pippin declares no relevant financial relationships with ineligible companies.

Disclosure: Vikas Gupta declares no relevant financial relationships with ineligible companies.

Post-infarction cardiosclerosis

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Post-infarction cardiosclerosis (PICS) is characterized by replacement of myocardial fibers with connective tissue and deformation of the valves. The disease is diagnosed 3–4 weeks after myocardial infarction and the completion of scarring of the connective tissue.

Etiology of the disease

Damage to the heart muscle results in the death of myocardial fibers and the formation of focal necrosis. Recovery occurs due to the growth of scar tissue, which causes violations of contractile function and prevents normal conduction of the myocardium. The condition is accompanied by arrhythmia and hypertrophy of a vital organ with the development of chronic heart failure. In the postinfarction period, cicatricial processes can affect the heart valves, which leads to their deformation and dysfunction.

Symptoms

The main cause of PICS is myocardial infarction, and clinical manifestations depend on the localization and prevalence of the process. The smaller the area of ​​functioning myocardial tissues, the more likely it is to develop arrhythmias and heart failure. PICS is manifested by characteristic symptoms, usually observed:

• shortness of breath, including at rest;
• cardiac arrhythmias;
• peripheral edema;
• pressing pains in the myocardium;
• decreased exercise tolerance;
• increased fatigue.

Particularly dangerous are sclerotic changes in the conduction pathways, in which heart rhythm disturbances develop. In severe cases, recurrent ventricular tachycardia is observed, in which the probability of death is high.

Diagnosis and treatment

After a heart attack, the diagnosis of PICS usually does not cause difficulties and is confirmed by anamnestic data, ECG, echocardiography, scintigraphy and coronography.

The purpose of conservative therapy of patients suffering from postinfarction cardiosclerosis is to improve the functional state of the myocardium, slow down the progression of heart failure and conduction disturbances, and prevent arrhythmias. The complex therapy includes the following groups of drugs:

• ACE inhibitors;
• beta blockers;
• diuretics;
• metabolic agents;
• extended release nitrates.

Severe conduction and cardiac arrhythmias may be indications for surgical operations. The implantation of a pacemaker or cardioverter-defibrillator is usually considered. For angina pectoris, angioplasty, stenting, or coronary artery bypass grafting is performed.

An important condition for maintaining health is maintaining a healthy lifestyle, changing the diet, limiting physical and psycho-emotional stress, regular visits to a cardiologist.

symptoms, classification, causes and methods of treatment in “SM-Clinic”

This disease is treated by a Cardiologist

• About the disease
• Species
• Symptoms
• Causes
• Diagnostics
• Expert opinion
• Treatment
• Prophylaxis
• Rehabilitation
• Questions and Answers

Types of post-infarction cardiosclerosis

The classification of post-infarction cardiosclerosis includes two types of morphological picture with sclerotic changes against the background of a heart attack. If areas of fibrous tissue form scars, a focal type is diagnosed. With a uniform distribution of altered tissue areas on the myocardium, we are talking about diffuse sclerosis.

On examination, the scar type can be identified by whitish areas that can penetrate into the deeper layers of the organ. Diffuse changes are less noticeable, but the myocardial stroma becomes thicker, coarser.

Symptoms of post-infarction cardiosclerosis

Post-infarction cardiosclerosis can be detected during examination. It is not he who has clinical manifestations, but the heart failure associated with it, which is manifested by the following symptoms:

• dizziness and fainting;
• fatigue;
• chest pain;
• edema;
• cough;
• shortness of breath.

The difficulty of timely detection of cardiosclerosis lies in the fact that some patients suffer a heart attack imperceptibly, attributing the manifestations of a dangerous condition to fatigue, age, and the body’s reaction to the weather.

Symptoms of post-infarction cardiosclerosis do not appear immediately: it takes time, on average, 2-3 months for the formation of cicatricial changes. Depending on which areas of the myocardium suffered more during a heart attack, the main signs of sclerosis may include:

• conduction disturbance: dizziness, fainting;
• tachycardia, atrial fibrillation;
• edema in right heart failure;
• shortness of breath and pallor with left heart failure.

Dysfunction of the heart muscle affects the blood supply to all organs, so the clinical picture of the disease may include other manifestations.

Causes of post-infarction cardiosclerosis

Post-infarction cardiosclerosis is a natural consequence of a cardiovascular accident, i. myocardial infarction. The amount of scarring depends on the volume of the affected tissue.

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If you experience these symptoms, we recommend that you make an appointment with your doctor. Timely consultation will prevent negative consequences for your health.

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Why SM-Clinic?

1

Treatment is carried out in accordance with clinical guidelines

2

Comprehensive assessment of the nature of the disease and treatment prognosis

3

Modern diagnostic equipment and own laboratory

4

High level of service and balanced pricing policy

Diagnosis

The standard list of studies after a heart attack and to identify associated sclerosis of the heart muscle include:

• electrocardiogram;
• echocardiography;
• Holter ECG monitoring;
• ambulatory blood pressure monitoring;
• coronary angiography.

Laboratory examination is necessary to assess general health and includes clinical and biochemical blood tests. It is aimed at identifying complications in the liver and kidneys, as well as monitoring lipid profile indicators to assess the likelihood of having a second heart attack.

Expert opinion

The death of the patient can be a consequence of post-infarction cardiosclerosis. Aneurysm, blockade, atrial fibrillation, acute ischemia are only some of the complications that a person faces who has not received the necessary medical care for a heart attack on time. Some patients cannot exist without oxygen support, therefore, in fact, they become disabled.

Cardiosclerosis is irreversible, so the patient needs to change his lifestyle immediately after discharge from the hospital. Attempts to return to previous activity often result in readmission to the hospital. The greater the load on the heart, the more the connective tissue foci will spread, and the worse the patient’s prognosis will be.

Kokorin Ilya Alexandrovich

Cardiologist, Ph.D. Deputy chief physician for the polyclinic at the SM-Clinic in Staropetrovsky proezd

Treatment of post-infarction cardiosclerosis

The treatment prescribed by a doctor for post-infarction cardiosclerosis is aimed at maintaining the functional state of the preserved tissues of the heart muscle, stopping the symptoms of manifestations of heart failure and arrhythmia.

Conservative treatment

Drugs for postinfarction cardiosclerosis include:

• antihypertensive drugs to normalize blood pressure;
• beta blockers to decrease heart rate and relax the heart muscle;
• diuretics to increase the effectiveness of blood pressure medications.

It is possible to support the part of myocardial tissues undamaged by sclerotic changes with the help of antihypoxants. They are aimed at reducing oxygen starvation of cells and eliminating its consequences. The prescription plan may include cardioprotectors, antioxidants, B vitamins, potassium, and magnesium.

Further treatment is aimed at maintaining the health of the cardiovascular system, preventing re-infarction. It includes taking medications, including those to lower blood cholesterol, and lifestyle changes:

• giving up bad habits;
• daily moderate physical activity;
• correct daily routine, enough hours of sleep;
• maintenance of optimal body weight;
• mental hygiene.

Under the control of a regularly conducted coagulogram, it is recommended to take drugs to prevent thrombosis.

Surgical treatment

If post-infarction cardiosclerosis has caused a violation of the electrical conduction of the heart, the patient is shown to install a pacemaker. The procedure takes place under anesthesia or local anesthesia, with access to the heart through the arteries. The rhythm stimulator will prevent the development of arrhythmia, tachycardia, cardiac arrest.

In case of an aneurysm (thinning of tissue with a bulging part of the wall) of the heart, resection of the affected area may be required, with simultaneous performance of coronary artery bypass grafting.

Prevention of postinfarction cardiosclerosis

Postinfarction cardiosclerosis can be prevented by maintaining a healthy cardiovascular system. According to statistics, the cause of a heart attack is often not genetically determined factors, but lifestyle. Therefore, it is possible to avoid a dangerous cardiovascular catastrophe by quitting smoking, alcohol and physical inactivity, maintaining body weight within the limits of BMI knowledge, and annual medical examination.

Secondary prevention, necessary to prevent re-infarction and the associated spread of connective tissue foci, is the full implementation of all medical prescriptions.

Rehabilitation

A modern approach to the surgical treatment of heart diseases allows making operations minimally invasive. Therefore, a long recovery after them is not required. The patient spends 1-2 days in the hospital, and if he feels satisfactory, he can return home.

During the first year after a heart attack, when the heart is trying to restore functional activity, overwork and stress should be avoided. A sanatorium, sparing lifestyle is recommended. You can return to work, if it is not associated with physical activity, after 1-3 months, depending on the state of health and the degree of myocardial damage.

Questions and Answers

Postinfarction cardiosclerosis is only caused by ischemic infarction, but sclerosis can also cause injury or inflammation. If a person has survived a heart attack, foci of scar tissue in his heart will remain forever. But the sooner he received help, the smaller the area of ​​the scar.

Excision is only indicated for thinning of the heart muscle tissue. Removing the scar does not make sense: firstly, it will not restore the disturbed electrical conductivity of the tissues, and secondly, the procedure again injures the myocardial tissue.

Khorolets Ekaterina Viktorovna Postinfarction cardiosclerosis against the background of concomitant pathology // Chief Physician of the South of Russia. 2019. No. 1 (65).

Shvalb PG, Obidin AV Verification of postinfarction cardiosclerosis by coronary angiography // Ros. medical biol. vestn. them. acad. I.P. Pavlova. 2004. No. 3-4.

Shugushev Z.Kh., Rudman V.Ya., Patrikeev A. V., Maksimkin Daniil Aleksandrovich, Baranovich V.Yu., Veretnik G.I., Mambetov A.V. Endovascular interventions in patients with postinfarction cardiosclerosis // Bulletin of the National Medical and Surgical Center. N. I. Pirogova. 2014. №3.

Shurygin Mikhail Gennadievich Patterns of changes in intracardiac hemodynamics in the development of postinfarction cardiosclerosis // BMZH. 1997. No. 3.

Patrikeev A. V., Rudman V. Ya., Maksimkin Daniil Aleksandrovich, Mambetov A. V., Veretnik G. I., Baranovich V. Yu., Faybushevich A. G., Shugushev Z. Kh. Possibilities for improving the prognosis of patients with postinfarction cardiosclerosis // Russian Medical Journal. 2015. №3.

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Myocardial hypertrophy
Hypercholesterolemia
myocardial infarction
Ischemic heart disease (CHD)
Cardialgia
cardiomyopathy
Atrial fibrillation
Myocardial dystrophy
Myocarditis
Mitral insufficiency
mitral stenosis
Conduction disorders of the heart
Heart rhythm disorders
Aortic valve insufficiency
Cardiopsychoneurosis
Pericarditis
Heart disease
rheumatic heart disease
cardiac asthma
Heart failure
Wolff-Parkinson-White Syndrome (WPW)
Marfan syndrome
Obstructive sleep apnea syndrome (OSAS)
arterial stenosis
Angina pectoris (angina pectoris)
Tachycardia
Extrasystole of the heart
Endocarditis

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VDNKh metro station

Belorusskaya metro station

Lesnaya, d. 57, bld. 2 Sevastopolskaya metro station

Chertanovskaya metro station

Krylatskoye metro station

Voikovskaya metro station

Staropetrovsky proezd, 7A, building 22

st. Clara Zetkin, 33 bldg. 28

Baltiyskaya metro station

Staropetrovsky proezd, 7A, building 22

st. Clara Zetkin, 33 bldg. 28

Maryina Roshcha

Novye Cheryomushki

Vodny Stadion

Ulitsa 1905 Goda

Yugo-Zapadnaya

Sukha revskaya

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